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Interstitial Gingivitis

SO-CALLED PYORRHEA ALVEOLARIS

EUGENE hi. TALBOT, M. D., D. D. S.

Pkofessok of Dental and Dual surgery, Northwestern I'nivf.rsity. Woman's .Medical
Honorary President of the Dental Section of the Tenth International Medical Congress,
Berlin, 1890; Honorary President of the Dental Section of the Twelfth International
Medical Congress, Moscow, 1897; Honorary Secretary of the Pan-American Medical
Congress. Washington. 1893; Member of the American Medical Association; Fellow
of the Chicago Academy of Medicine; Member of the Chicago Medical Society;
Secretary of the Section on Stomatology of the American Medical Asso-
ciation; Member of the Chicago Academy of Sciences; Honorary Member
of the odontologischen gesellschaft, berlin, germany; membre
Honoraire de l' Association Generale des Dentistes de France;
Honorary Member Sociedad Odontologia Kspanola; Author of
"The Irregularities of the Teeth and their Treatment"
Author of " Chart of Typical Forms of Constitutional
Irregularities of the Teeth"; Author of "The Eti-
ology of Osseous Deformities of the Head, Face,
Jaws and Teeth". Author of "Degeneracy, its
Causes. Signs and Results"; Kic. I'm-

with seventy-three illustrations.

PHILADELPHIA:

THE S. S. WHITE DENTAL. MANUFACTTJB.ING < < >.

1 899.

Entered According to Act of Congress, in the Year 1899, by

Eugene S. Talbot,
the Office of the Librarian of Congress at Washington, D. C.

ALL CO-WORKERS IN DENTAL SCIENCE,

This Work,

As a Slight Token of Appreciation of Their Contributions to Science,

is Respectfully Dedicated.

Digitized by the Internet Archive

in 2012 with funding from

LYRASIS Members and Sloan Foundation

http://archive.org/details/interstOOtalb

PREFACE.

The great law of medical science, that to know the cause is
half the treatment, is as applicable to dentistry as to any other
specialty of medicine, and is as applicable to dental problems as
to those of biology generally. Treatment of any disease without
knowledge of its pathology is practically a failure.

While much has been written upon the pyorrhceic stage of
interstitial gingivitis and its treatment, during the past two
decades, no new principle has been advanced whereby the parts
can be restored to a healthy condition, or whereby the disease
can he prevented. The disease is admittedly on the increase.
This seems at first sight to indicate that dental prophylaxis and
treatment, so tar as this disease is concerned, is a failure.

Other specialists restore patients to health. Nearly every
patient with this disease applies to dentists. Most dentists, how-
ever, hardly know the disease exi.--.ts and much less arc capable
of ottering suggestions as to treatment. It seems strange that in
America so little original work has been done upon a disease
more to be dreaded than tooth decay. Treatment has been
wholly at random, and hence, as a rule, only to limited extent
successful. Destruction of the alveolar process and loss of the
teeth is so rapidly sure that the necessity for dental scientists to
solve the etiology of this very common disease seems imperative.

Nearly two decades ago I felt and expressed the necessity for
more extended study (Dental Cosmos, 188(5, page C>S ( .)) of the
clinical aspects and etiology of this disease. Even during appar-
ently diverse and separated studies, such as those related to dental
and maxillary irregularities and degeneracy, the necessity for
this has forced itself still further upon me. In the present
study, the disease has, of necessity, been considered from the
broad standpoint of general pathology. In all instances where
possible personal elements of error are present, these have been
eliminated bv having researches made bv more than one observer.

The attempt has been made to summarize all researches on
the subject. So much have opinions been intermingled that it is
possible that proper credit for priority has unintentionally not
been given.

The author is under obligation to the following scientists for
their kind assistance : Dr. Ludwig Hektoen, Pathologist, Rush
Medical College ; Dr. Jerome H. Salisbury, Chemist, Rush
Medical College ; Dr. W. A. Evans, Pathologist, Columbus Med-
ical Laboratory, Professor of Pathology, Chicago College of
Physicians and Surgeons and Milwaukee Medical College ; Dr.
J. A. Wesener. Chemist, Columbus Medical Laboratory, Profes-
sor of Chemistry, Chicago College of Physicians and Surgeons ;
Dr. Vida A. Latham, Pathologist, Northwestern University,
Woman's Medical School; Dr. Maximilian Herzog, Pathologist,
Chicago Polyclinic Hospital ; Professor Theo. A. Edwin Klebs
and Dr. Robert F. Zeit, Pathologists, and Dr. W. L. Baum,
Professor of Diseases of the Skin, Post-Graduate Medical School,
Chicago ; Dr. G. V. I. Brown, Professor of Oral Surgery, Dental
Department, Milwaukee Medical College; Dr. Frederick Noyes,
Histologist, Dental Department, Northwestern University ; Dr.
J. G. Kiernan, and to Blomgren Bros. & Co. for electrotypes, etc.

THE AUTHOR.
103 State Street, Chicago.

CONTEXTS.

CHAPTER. PACK.

I. History . . . . . . . .1

II. Introduction ........ 10

III. Transitory Structures —

The Jaws * . .2(1

The Alveolar Process ..... 21

Periosteum and Peridental Membrane . 33

The Gums -and Mucous Membrane ... 42

Do Glands Exist in Epithelial and Peridental Mem-
brane? ........ 47

Bone Building and Absorption .... 59

IV. Theories of Interstitial Gingivitis . . . .65
V. Uric Acid and Interstitial Gingivitis ... 68

VI. Inorganic Salts and Interstitial Gingivitis . . 73

VII. Heredity and Environment ..... 83

VIII. Degeneracy and Degenerate Tissues . . . .86

IX. Neurotic, Diathetic and Degenerate Children . . 89

X. Interstitial Gingivitis in Dogs . . . . .98

• XI. -Mercurial Interstitial Gingivitis in Dons . 117

XII. Bacteriology of Interstitial Gingivitis . . . 122

XIIL Scorbutic Interstitial Gingivitis in Man . . . 127

XIV. Interstitial Gingivitis in Man from Metallic and Other

Drug Action . . . . . . .142

XV. Conclusions . . . . . . . .146

Pathogenesis of Interstitial Gingivitis . . 151

Endarteritis Obliterans ..... 154

Absorption of the Alveolar Process . . . 157

Pyorrhcka Alveoi.aris from Interstitial Gingivitis . 162
Constitutional Effects of Pyorrhcea Alveolaris . 167
Calcic Deposits ....... 168

XVI. Treatment . . . ... . .172

INTERSTITIAL GINGIVITIS.

CHAPTER I.

HISTORY.

Inflammation of the peridental membrane is probably coeval
with man. Some of the skulls found earliest in the cave-dwell-
ing period exhibit evidences of its presence. In some of these,
careful observation lias shown deposits encroaching upon the
roots of the teeth and resultant absorption of the alveolar
process.

In the Swiss lake-dwellings and in the earlier Irish cran-
noges of like construction and situation, skulls are found, which
exhibit deposits of tartar, inflammation of the peridental mem-
brane and al (sorption of the alveolar process. These skulls were
those of primitive races in whom disease of the jaws and teeth i-
supposed to he absent or infrequent. In the skulls of the peo-
ples exhibiting the highest civilization at the earliest period —
those of the Accadians and Egyptians — similar inflammatory
conditions are to be found. This, however, was to have been
expected, to judge from the dental directions left among the
medical records of these peojjies. The Greeks, Syrians, Arab-
ians, Dravidians and Aryans of India and the early Burmese
all suffered from this disorder. In the museum at Constan-
tinople are the skulls of soldiers who fought at a battle 328
B. C. One of these skulls has the anterior alveolar process
entirely absorbed away. The roots of the right central, the
right lateral and the left central incisors are exposed.

Inflammation of the peridental membranes, it will be evident,
is, therefore, not a modern disease; not a disease confined either
to civilized or primitive races, hut one which attacked man early

Z INTERSTITIAL GINGIVITIS.

in his evolution. Like most diseases it has been chiefly dis-
cussed and analyzed during the past two centuries.

In 1740 H. A. Fauchard ' (while recognizing the disease in
all its essential features and describing its principal symptoms)
advanced no theory as to its origin.

In 1778 M. Jourdain 2 advanced the opinion that the disease
was of scorbutic origin.

In 1821 L. Kaecker 3 discussed the disorder in an essay on
the devastations of the gums and alveolar processes.

In 1822 M. Joirac 4 (in a discussion of the disease), Avhile
advancing no theory as to its origin, called it " pyorrhoea inter-
al veolo-dentai re. ' '

In 1860 Marshall de Calve 5 advanced the opinion that the
disorder was of hereditary origin.

In 1867 Magitot, discussing the disorder, advanced the
opinion that the gum, being in all cases only attacked subse-
quently, is not the original seat of the lesion. In his opinion
systemic disorders like gout, rheumatism, albuminuria, diabetes
and anaemia had an influence.

Bonwill 6 during the same year expressed the opinion that
the disorder was due to thinness of the alveolar process between
the teeth, thus depriving the peridental membrane and gum
tissue of proper support, The want of proper articulation of
the teeth also exerted an influence.

In 1870 Brown ascribed the disorder to seminal calculus.

In 1875 John T. Riggs, after whom the disorder is frequently
called, entitled it (in a paper read before the American
Academy of Dental Surgery) suppurative inflammation of the
gums and absorption of the gums and alveolar process.

During the same year Scheff 7 of Vienna entitled the disorder
periostitis dentalis. He was of the opinion that it originated
from external irritation through mechanical, thermic and chemic
changes. The real origin of the disorder was, in his opinion,

1 Independent Dental Journal, 1875.

2 Philadelphia Journal of Medical and Physical Science, 1821.

3 International Dental Journal, Vol. XIII.

4 Journal of the American Medical Association.

5 Journal of the American Medical Association.
G Dental Cosmos, Vol. XXIV.

7 Wiener Med. Presse, Vol. XVI.

very often obscure. He doubted, however, the influence of
rheumatism.

In 1876 Sirlctti ' ( in a discussion of the pathology of the
disorder, which he called alveolo-dental periostitis) regarded it as
due to constitutional conditions, like rheumatism, scrofula, syph-
ilis, etc., with local causes as exciting factors.

In 1S77 Rehwinkle, 2 in a paper on pyorrhoea alveolaris, after
citing from Albright (of Berlin) the claim that the disorder
was due to unclean liness, mercury and the suppression of habitual
secretions, expressed the opinion that acquired and inherited
constitutional defect often played an important part as etiologic
factors. He was also of opinion that mercury exerted an influ-
ence in its causation. Salivary deposits were, in his opinion,
without influence. Clowes 3 was of opinion in 1879 that the
general cause was lack of nutrition in the parts. The use of
wedges often excited the disorder.

C. J. Essig, 4 in 1880, expressed the opinion that its predis-
posing causes were unknown, that it occurred as a rule in healthy
persons, and that irregular and crowded teeth acted as an exciting
cause.

In another paper during the same year G. A. Mills 5 expressed
the opinion that the disorder was of systemic origin. Various
mental and physical influences aided its progress, such as nervous
exhaustion and bodily and mental overwork. In his opinion it
frequently occurred in children and adolescents from eruptive
fevers. The deposit was only a local manifestation of the
disorder.

In 1881 X. S. Niles 6 expressed the opinion that constitutional
conditions were, as a rule, without influence, and that local irrita-
ting deposits were the cause in twenty-five per cent of the cases
coming under his observation. He was of opinion also that the
amount of lime salts taken into the system in drinking water
exerted an influence. A calcic and phosphatic diathesis had an
influence in the production of the disorder.

■Gazzetta Medica di Roma, ls7(i.
-Dental Cosmos, Vol. XIX.
'Ibid., Vol. XXI.

4 Dental Cosmos, Vol. X XI.

5 Ibid., Vol. XXIII.

6 Ibid., Vol. XXIV.

4 INTERSTITIAL GINGIVITIS.

In 1881 (when there seemed to have been many contributions
to the literature of the subject) Atkinson 1 expressed the opinion
that nervous debility or original defect in innervation exerted an
influence in the production of the disorder. The deposits of
tartar were a secondary consequence. In the course of his paper
he cited the opinion of Hamilton Cartwright that Riggs's disease
commenced in an unhealthy condition of the gums with a sec-
ondary deposit of tartar.

In a paper read before the Dental Section of the Inter-
national Medical Congress, Walker 2 claimed that the starting
point of the disease was subacute inflammation passing into the
depths of the alveolar process adjacent to the inflamed gum. In
the discussion of this paper, Archovy and Joseph Izklai, of
Buda Pesth, ascribed the disorder to minute organisms. Oakley
Coles thought that systemic states were the predisposing factors,
while minute organisms exerted an exciting influence.

In 1882, L. C. Ingersol 3 regarded sanguinary calculus as a
manifestation of the disorder, and distinguished it from salivary
deposits.

Malasses and Gallippe, 4 in 1884, expressed the opinion that
the disorder was of microbic origin.

In 1885, A. O. Rawls 5 expressed the opinion that the causes
were environment with morbid factors, such as malaria, excessive
sodium, etc., chloride and mercury.

In 1886, Reese 6 expressed the opinion that the disorder had
its source in the uric acid diathesis resultant on abuse of
alcohol.

During the same year, J. D. Patterson 7 expressed the opinion
that the disorder was of catarrhal origin. Later, in 1886, J. N.
Farrar 8 regarded the disorder as a combined result of systemic
tendencies and local irritants. There was a peculiar condition of
the system associated with hypersecretion laden with increased
earthy deposits.

1 Dental Cosmos, Vol. XXIV.

2 Transactions of the International Medical Congress, 1881.

3 Dental Cosmos, Vol. XXV.

4 Ibid., Vol. XXVI.

5 Ibid., Vol. XXVII.

fi Independent Practitioner, Vol. VI.

7 Dental Cosmos, Vol. XXI.

8 Independent Practitioner, Vol. VII.

A. R. Starr later also expressed the same opinion. He, how-
ever, was unable to determine the local irritation factor, but
regarded it as the same as that which causes exostosis of the
cementum. He had found most cases in the upper jaws.

Black 1 designated the disorder phagadenic pericementitis. It
was a specific infection of an inflammatory character, having its
origin in the gingiva, and was accompanied with destruction of
the peridental membrane and alveolar walls.

E. S. Talbot J during the same year regarded the disorder as
a local one, due to both local and constitutional causes. The
disorder began with simple inflammation of the gums, which
afterward became chronic.

Of the status of this disease at the close of the year 1887,
the following analytic picture was drawn by W. X. Sudduth 3 :
Pyorrhoea alveolaris is a term applied to the secondary stage- of
a disease that has its inception in a catarrhal stomatitis. Being
confined, as a rule, to the margin of the gums surrounding the
teeth, it might be called a " gingivitis," w T ere it not for the gen-
eral catarrhal tendency shown by the entire mucous membrane
of the mouth and nasal passages. The intimate relation between
a general catarrhal idiosyncrasy and pyorrhoea alveolaris is more
than mere coincidence. Its common occurrence in persons who
have irregular teeth has also been often noted by Dr. Sudduth.
who considers that this fact has, besides the matter of uncleanli-
ne>s, a direct bearing upon its pathogeny. It is well known that
the irregularities of the teeth present an indication of a degener-
ative taint, and that persons in whom irregularities occur are
very prone to catarrhal affections of the respiratory organs,
including the nasal passage. Their skin is usually very suscep-
tible to inflammatory affections. Another feature is offensive
odor of the saliva of individuals who show this particular ten-
dency to catarrhal affections even in persons who take most scru-
pulous care of the teeth. In the majority of cases, pyorrhoea is
a stomatitis in which the local and constitutional factors in the
production of the disease are largely dependent upon hereditary
catarrhal dyscrasia for their ability to engraft themselves upon

1 American System of Dentistry.
-' Dental Cosmos, Vol. XXVIII.
; Sajous' Annual, 18S8, Vol. Ill, page 365.

b INTERSTITIAL GINGIVITIS.

the tissues. This position is borne out by the clinical experience
of Patterson, of Kansas City, Missouri, who reports thirty-eight
cases of well marked pyorrhoea observed by him, thirty-three of
which presented undoubted evidence of nasal catarrhal condi-
tions ; two were the result of direct irritation of misfitting partial
plates, and the remaining three were apparently caused by cal-
cific deposits. Patterson remarks that a close examination of the
history of the above quoted cases confirms the opinion that the
disease is, as a rule, an " oral catarrh."

From the foregoing W. X. Sudduth feels justified in class-
ing the disease as a localized catarrhal stomatitis which may be
either acute or chronic. Acute catarrhal inflammation of the
gums begins in circumscribed points which present a bright or
rose-red color, and which are generally located on the margin or
the rugse of the palate. There is but little swelling because of
the dense nature of the sub-epithelial connective tissues. The
gums present the same stages as are found in inflammation of
other mucous surfaces — first dryness, followed by an increased
secretion of mucus. The parts are very sensitive to pressure;
the patient complains of an annoying, burning sensation. The
appearance of the gums is noticeably smooth and glistening.
They bleed easily when the brush is used or even during a meal.
This stage does not last very long, but soon heals by resolution
or passes into a chronic catarrhal stomatitis in which condition
the gums become markedly swollen and turgid. They present a
condition of tumefaction that sometimes rapidly passes into
hypertrophy ; at other times there is an indurated appearance
that may last for some time. Granulation tissue may be pro-
duced as the result of overstimulation. The gums become
detached from the necks of the teeth ; and pockets are formed
from which a fetid discharge may be pressed, giving a peculiarly
disagreeable odor. Bulla are apt to form, which, by rupturing
in the process of mastication, give rise to intense smarting. The
tongue constantly seeks the surface if it be on the inner side.

The pathologic changes which take place are, according to
Newland Pedley, of England, "hypertrophy of the muco-peri-
osteal fold around the teeth, accompanied by dilatation of capil-
lary loops, enlargement of the papillae and rapid proliferation of
epithelial cells. Later the gums become firm and contracted and

display increase of fibrous tissue. The changes which go on in
the socket have not been as yet satisfactorily worked out. The
examination of the jaws of earnivora, apparently affected with
pyorrhoea alveolaris, leads to the supposition that osteitis of the
alveolar process spreading toward the apex of the socket is pres-
ent. Later the alveolar walls become absorbed and are at times
more or less denuded, while the fangs of the teeth become coated
with a layer of thin, hard, green-brown tartar. Ultimately the
disease progressing, the teeth, one after another, drop out."

From what has been said it will be seen that the pathology
of pyorrhoea alveolaris may be explained in several ways. The
general causes are local or symptomatic, or both combined. The
most common cause of catarrhal gingivitis is found in local
irritation, combined with some hereditary disposition to catarrhal
affections. The next greatest etiologic factor is symptomatic —
the local manifestation of a constitutional vice. The most com-
mon manifestation is that of syphilis and of its antidotes, mercury
and potassium iodide, both of which sometimes find expression in
a localized inflammation which may be the starting point for
pyorrhoea alveolaris. As a complication of the disease in its
secondary stages there can be no doubt of the action of micro-
organisms, but Sudduth does not feel justified in conceding to
them a position of specificity.

His position above quoted is sustained by Pedley, who finds
that in most instances it is due to some constitutional condition.
The fact that it is often symmetrical and frequently hereditary
gives support as to this view. It occurs in mouths of patients
whose health has been undermined by debilitating influences and
injudicious habits of living. It is a common sequel of malarial
fever. Young persons recovering from eruptive fevers are some-
times subjects of pyorrhoea alveolaris. Frequent pregnancies are
a fruitful source of the disorder. Attention has been lately
drawn to the shedding of the teeth in tabes dorsalis, but it does
not, however, seem to be a constant symptom. Pedley 's view.
although tending entirely toward the constitutional character of
the disease, does not militate against its catarrhal nature.

Bland Sutton has found shedding of teeth frequent in rheu-
matoid arthritis in animals. He has also met with it in mollities
ossium and other wasting diseases. Magitot (who views the

8 IXTEKSTITIAL GINGIVITIS.

alveolar dental periosteum as a ligament and not of the same
nature as osseous periosteum) calls the disease symptomatic
alveolar-arthritis, and mentions especially as causes, chronic
Bright' s disease and glycosuria, in which latter condition the
phenomenon is absolutely constant.

Patterson holds that " mouth-breathing has, in his expe-
rience, been a very common accompanying condition which he
cannot help connecting with the production of the disease. By
it the gums are kept dry, their functions destroyed and the way
paved for catarrhal inflammation. The majority of the patients
he has been called upon to treat have been otherwise healthy,
robust persons. From this fact he does not favor the idea of the
disease being dependent upon constitutional derangement. It
is, however, a well-known fact that these are the very class of
people who when irritation is once set up in their system, present
the most aggravated cases, by reason of their superfluous vitality.
He says he has occasionally met with cases where the local con-
dition was evidently aggravated by constitutional derangement
and cure was thereby retarded. The great majority of cases,
however, have shown no indication of constitutional predisposi-
tion, but have pointed unerringly to local irritation by means of
which the function of the mucous membrane had been destroyed."

Syphilis and other affections may engraft themselves upon
the gums without a predisposition of the parts toward an inflam-
matory condition, and having disturbed the normal status of the
gingival margins they pave the way for subsequent disease in
the alveolus. Certain drugs, such as mercury, phosphorus, lead,,
etc., have a known deleterious action upon the ligamentous
attachment of the teeth.

In 1890 Miller 1 expressed the opinion that the disorder was
of a parasitic nature.

In 1892 C. N. Pierce 2 charged the disorder chiefly to sys-
temic predisposition and enthusiastically advocated the theory of
Reese as to the influence of the uric acid diathesis. In 1894
W. X. Sudduth 3 strongly urged the influence of lactic acid as a
local factor in the disorder.

Micro-Organisms of the Human Mouth.
International Dental Journal, Vol. XIII.
'Ibid., Vol. XIV

John Fitzgerald, 1 in 1899, claimed that "The production of
pyorrhoea depends upon two factors, a predisposing cause and
a local irritation. The predisposing cause may be tubercle,
syphilis, scurvy, the exhaustion of acute infectious di>e;i>r> or
any other source of malnutrition. The exciting cause may be,
and most usually is, a gingivitis produced in one of the ways to
be presently described. There is also a pyorrhoea of gouty
origin, in which the local necrosis of the peridental membrane is
caused by gouty disease of one of the blood vessels in its sub-
stance."

The views on etiology of this condition have varied, it will
be observed, from purely constitutional causes to purely local
causes, inclusive of microbic affections. In the main it will
be obvious, however, that both constitutional causes, whether
inherited or acquired, have been regarded as of influence by the
majority of those who have written on the subject. There has,
however, been very little exact study of either the predisposing
or the exciting causes of the condition. Even the impetus given
the study of etiology by bacteriology and embryology has as yet
failed to make itself felt to any considerable degree in this
department of dental pathology.

'Clinical Journal, March 1, 1899.

CHAPTER II.

INTRODUCTION.

The attempt has been made in the present work to reduce to
order the chaotic notions as to etiology, pathology and treatment
which, during the present century, have gathered around the
morbid condition erroneously entitled Pyorrhoea Alveolaris.
While even erroneous titles may have their meaning so fixed by
usage that any danger from the error involved in the title may
be practically nil, still this is not the case with the title just
cited. It suggests erroneous etiology, since pyorrhoea implies
that there must always be a flow of pus, and hence that the dis-
ease must always result from infection with pus microbes. It
implies erroneous pathology and erroneous treatment for the
same reason. This being the case, such a title is so dangerously
misleading as to compel in the present stage of dental science its
complete disuse. With a view of clearing up this question at
the outset by the use of a proper title, I have adopted as a desig-
nation for the condition hitherto known as pyorrhoea alveolaris,
the term "Interstitial Gingivitis." To this designation (as to all
other attempts to express within a small space an extended path-
ology, etiology, prognosis, and clinical aspects) there are some
objections. The term interstitial is used by some pathologists in
a limited obscure sense. By the mass of dental pathologists,
surgeons, physicians, and by medical lexicographers, the term is
employed in precisely the sense in which it is used in the present
work. The English surgeon and lexicographer Quain defines
interstitial as follows : " Interstitial (inter, between ; and sto, I
stand) ; relating to the interstices of an organ. The term is
applied in physiology to the tissue which exists between the
proper elements of any structure, namely, some form of connect-
ive tissue. In pathology the word is used in connection with
absorption when a part is gradually removed without any obvious

INTRODUCTION. 11

breaking off, and also to indicate the implication of the intersti-
tial tissues in morbid processes or their infiltration with morbid
products, as interstitial pneumonia, interstitial hepatitis."

The Encyclopaedic Medical Dictionary of the American
Foster, states that interstitial has three significations : First, it is
applied to a condition disseminated through the substance of an
organ or part, and to an inflammation affecting the connective
tissue of an organ ; second, it is also applied to that form of
growth which consists in the interposition of new elements
between old ones, instead of in addition to the surfaces ; third, it
is applied to pathologic processes occupying the space between
the essential parts of an organ which constitute its proper tissue,
and is then employed in a sense opposed to that of parenchy-
matous.

A glance at the illustrations demonstrates the validity of the
application of the term interstitial (in the sense of Quain, Foster,
and the other lexicographers) to the condition erroneously called
pyorrhoea alveolaris.

I have adopted the term gingivitis for reasons which will be
obvious at the first glance. The philologic objection may be
made that in it Greek and Latin are yoked together. Practically
this is no objection, since German, French, as well as English,
medical authorities employ such terms of mixed origin. Indeed
the French (Mailhol 1 for example) apply the term gingivitis to
the very condition to which I have applied it. In addition, they
add to it the specific term " expulsive," to designate " a form of
recession of the gums, accompanied by alveolar osteoperiostitis,
and the gradual expulsion of the tooth from its socket." Foster 2
suggests the substitution of the term ulitis as more philologically
correct. The term gingivitis, however, has crept into such wide
use, that it would be futile to attempt to displace it for merely
philologic reasons. The two terms I have employed convey a
fairly correct idea of the pathologic process involved, and do
not imply erroneous views as to etiology, pathology, prognosis
and treatment.

The pathologic conception adopted in the present work anent
interstitial gingivitis is that the disorder is a local inflammatory

1 Odontalgie.
- Foster, op. cit.

12 INTEESTITIAL GINGIVITIS.

condition of the gums, tending to accelerate their normal ten-
dency to disappearance at certain periods of stress, or involution,
of which involution the changes jDroduced by old age are a type.
In this early senility of the gums, for such it may be termed,
two great types of causes play a part ; the exciting and the pre-
disposing causes. The exciting causes may be purely local, or
may be local expressions of constitutional states. Thus it will
be shown that the influence of uric acid when present is exerted
as a local irritant, and not as a constitutional factor — the theory
urged so strongly by Pierce, whose views have been of late so
advocated by Kirk. 1 The uric acid hypothesis, once very domi-
nant in medicine, is now losing its force. The trend of medical
opinion is to consider it one of the danger signals of auto-intoxi-
cation which assumes prominence because of its tendency to
excite local irritation. It is but one of a number of local
expressions of constitutional defect. This view of the influence
of uric acid in etiology the present work will try to demonstrate.
Prominent among etiologic factors which have to be reckoned
with, are pathogenic germs. In the jn-esent work it will be
shown by all laws of bacteriology (under which investigations
must be conducted) that there is no specific germ which is caj)a-
ble of producing the disease itself, and furthermore, that the
pyorrhoea stage of the disease is merely a complication due to
pyogenic germ infection of the already diseased gums. The
views of Galippe as to a specific organism will be shown to have
failed of support by numerous control experiments described in
the present work. As these have been conducted by different
experimenters they are free from the personal elements of error
which vitiate the researches of Galippe, who violated that canon
of the laws of Koch which compels production of the disease by
the alleged specific germ. One predisposing factor will be
shown in the present work to be the nature of the structures
affected. This in pathology is called local predisposition. The
gums, etc., will be shown to be transitory structures in them-
selves predestined (as already stated) to certain changes at cer-
tain ages. By the influence of the disease, about to be discussed,
these changes occur prematurely. The influence of the toxic
agents (mercury, potassium iodide, etc.) will be shown to have

1 International Dental Journal, May, 1899.

INTRODUCTION. 13

been exerted constitutionally through the central nervous system,
their local effects being a secondary consequence of this. The
same will be shown to be the ease with conditions like scurvy
(where the constitutional factor is most prominent ), and with the
great neuroses (paretic dementia, locomotor ataxia, etc.). Here,
as in the toxic conditions, one great element considered is the
influence of the constitutional conditions upon the nerves gov-
erning local blood supply and tissne waste and repair. These
influences are significantly illustrated in the various processes
described later which tear down and build up.

The influence of morbid heredity as a direct factor will be
shown nut to lie great. The influence, however, of degeneracy
expressing itself along the lines of least resistance will appear
as an ominously important factor. Heredity here, as elsewhere,
is a warning rather than a destiny.

The influence of the nervous system on the processes of
growth and repair, which is called its trophic function, has been
shown to play a part in both the etiology of the disease and in
its progress. This function has received but little attention from
dentists, albeit its influence has been recognized in dental path-
ology in connection with great neuroses like paretic dementia
.and locomotor ataxia, in which gum disorders occur, followed by
loosening of the teeth. The pathology of the disease has been
discussed in the light of established facts of general pathology
which have been accepted by the leading dental investigators,
and not merely from a hypothetic standpoint. The disease has
been regarded as a local exaggeration of certain physiologic pro-
cesses, accompanied by diminution of the intensity of others. In
the study of this phase of the question, the latest researches of
dental pathologists as well as original observation and experiment
have been employed.

Among the many questions which the present treatise is
believed to settle (so far as experimentation can) is the following :
The question of the influence and nature of its etiology. It is
shown that here, as elsewhere in biology, the etiology of morbid
conditions has many phases; that in it exciting and predisposing
causes have alike to be considered ; that while causes may be
constitutional in origin they very often exert their action locally ;
that the disease is not a product of civilization nor a product of

14 INTERSTITIAL GINGIVITIS.

any one etiologic factor ; that there is no ground yet adduced
for believing the disease to be specifically infectious and due to a
germ of a specific nature ; that in it the germ infection occurs
as a consequence of existing disease, and is not the cause of
the morbid condition, but one of its stages : Pyorrhoea. The
experiments made, as well as the pathologic and clinical data,
have been obtained from many observers, so that as many control
observations should be had as were necessary to eliminate per-
sonal elements of error inevitable upon original observation and
research. In the pathology no statement is made which is not
demonstrated by corroboratory data, including a photograph of
the condition. The treatment has been based upon the pathology
and etiology. Its central idea is that the human being must be
regarded as something more than his mouth and teeth ; hence the
duty of the dental scientist is, like that of all medical scientists,
best shown in a prophylactic direction.

The pathologic material for the study of interstitial gingivitis
in man is obtained with such difficulty in the recent state as to
necessitate research upon animals. This disease was noticeably
present among the carnivora, casually inspected in American
and European zoologic gardens. Cats and dogs were also known
to be liable to the disease. As the first step in investigation, two
practitioners of comparative medicine, with an extensive hospital
practice (Dr. Charles E. Sayre and Dr.. Alsop E. Flower), were
consulted as to the frequency of this disease in animals. All
animals under their care suffered from it more or less, but eighty
per cent of dogs over eight years of age had the disease. Nearly
every dog in the hospital under their care was so affected. These
dogs comprised all breeds, from spaniels and terriers to the New-
foundland, St, Bernard and great Dane. On examination,
every phase of interstitial gingivitis was found in the mouths
of these dogs, from its inception to the loss of the teeth. The
number of dogs observed was twenty-seven. The roots of the
teeth of some were covered with deposits and so exposed that the
teeth could be removed with the fingers. Such diseased mouths
are rarely, if ever, present in human beings. The outer plate of
bone was absorbed, the roots entirely exposed, pus was oozing
from around them and the mucous membrane was badly inflamed.

It should be remembered that the jaw of the dog, like the jaw

[INTRODUCTION.

of man, is undergoing considerable variation. Like man, the
dog, having put himself under new social conditions (so to
speak), is varying greatly both as to brain, skull and jaw from
his wolf-like ancestor. As he is under the protection of man,
the struggle for existence as to food is less intense than in the

wild state and consequently there is less occasion, even for fight-
ing purposes, of his jaws and teeth.

Independently of conditions of this type, many of the dogs
suffered from constitutional disorders. Eight had skin diseases
which in the dog are more likely to produce obvious consti-
tutional defects than in man. Some were old and blind. Some
had been injured and were under treatment for wounds. Some

I NTEESTITIAL GINGIVITIS.

were suffering from rachitis, nervous diseases, and were over-
bred. Others were constipated or had germ types of diarrhoea.
One had kidney inflammation and bronchitis with high fever.
In short, these dogs, being house dogs, presented most of the
constitutional diseases to which man is liable.

The mouth of a Scotch terrier is shown in Fig. 1. The

molar and premolar had been removed with the fingers. The
cuspids and incisors are quite loose. There are large deposits
of tartar. The gum and alveolar process have been absorbed
nearly one-half the length of the roots of the teeth. In Fig. 2
is seen the mouth of a Boston terrier with the incisors and pre-
molars removed. There is extensive pyorrhoea. There are

i.\Ti;oi>r<Ti<>.\.

calcic deposits upon the cuspids and molars. There is recession
of the gums and alveolar process. In Fig. 3 is shown the mouth
of another Boston terrier. In it one premolar in the upper and
one on the lower jaw have been extracted. There is extensive
inflammation of the gum about the molar, cuspid and incisor
with large calcic deposits about the teeth. In Fig. 4 are shown

teeth covered with calcic deposit the entire length of the root.
These teeth were removed by the fingers from the mouths of two
dogs, one of whom was later obtained for scientific study. This
was all the material to be obtained from the hospital, since the
dogs were pets who had been placed under treatment by their
•owners.

18 INTERSTITIAL GINGIVITIS.

Through the courtesy of Pound master Hugh Curran, the
necessary material was obtained from the Chicago Dog Pound.
Here from four hundred to a thousand dogs are killed per week
during June, July and August each year. Ninety-five per cent
are mongrel curs leading a street life, hence neither luxu-
rious diet nor luxurious care can be charged with any disease
in them. They have, at least, plenty of outdoor exercise and
fresh air. Many, despite this reversion to the life of their wolf-
like ancestors, have skin diseases and are deaf and blind from
old age. The bodies were secured after death, at which time
examinations of the mouths were made. Five per cent of the
dogs entering the pound are of good breeds. These, if not called
for by the owners, are sold for a moderate price.

The dogs selected for the death penalty are collected in a
large box pen, leading out of which is a door through which they

ff rtftftftjt*

Fi(i. 4.

pass into an air-tight box. Communicating with this box is a
stove in which sulphur is burned with charcoal. The fumes
pass into the box and death is almost instantaneous and
painless. After they remain fifteen minutes, a door leading to
the air is'opened and the bodies are carted away. It was at this
time that access was had to them. The mouths were then exam-
ined. Such cases as 'were of interest were placed on one side
and the jaws removed from the bodies. Inside of one-half hour
the specimens were in a solution to be kept until desired for use.
Jaws (with interstitial gingivitis in all stages of progress, from
simple inflammation of the gums to the most extreme cases of
exfoliation of the teeth) were obtained in an abundance for
future studies. It is not an easy matter to ascertain the ages of
these animals. In a general way, it was found that inflammation
of the gums, especially about the canine teeth, was almost always
present in dogs over one year. About twenty-five per cent of

INTRODUCTION. 19

these dogs at four years of age had the disease, eighty per cent at
from eight to ten years, ninety-five per cent over twelve years of
age. Since I commenced my investigation (four years ago), I
have examined quite a large number of dogs about homes, but
have never found a dog over four years without this disease to a
greater or less extent. Many house clogs at one year had inflam-
mation of the gums. Dogs for infection and those used for mer-
eurialization were picked up in the streets.

Most of the dogs exhibited at the last three animal dog shows
held in Chicago were young, ranging from one to four years of
age. About twenty-five per cent would range four years to
eight. Three years ago, on a casual examination of their mouths,
interstitial gingivitis was found to lie common. Occasionally
recession of the gums and pyorrhoea alveolaris occurred. During
the last two years, on more careful examination, twenty-five per
cent of dogs between the ages of one and four were found to have
interstitial gingivitis and seventy-five per cent of dogs from four
to eight years were found to have interstitial gingivitis with
recession of the gums and pyorrhoea alveolaris. In the study of
this disease, therefore, dogs are excellent substitutes, since for
pathologic research they can be obtained at any stage of the
disease.

CHAPTER III.

TRANSITORY STRUCTURES.
THE JAWS.

Because of man's advance in evolution and because of the
local degeneracies thereon resultant, through the law of economy
of growth whereby one structure is sacrificed for the benefit of
the organism as a whole, the face, jaws, teeth, gums, alveolar
process and peridental membrane, being variable structures, are
predisposed to disease in their very order of evolution.

The jaws are growing smaller because large ones are not
required. The structures are changing their shapes to adapt
themselves to the new environment. Thus — instead of broad
large jaws with low vaults; short, broad alveolar processes with
plenty of blood supply and vitality to resist mastication ; teeth
short, with large bell crowns to give plenty of room between the
roots for considerable thickness of the alveolar process for the
nourishment of the peridental membrane and support and pro-
tection of the gum tissue — small narrow jaws occur with appa-
rently high vaults ; long, slender and thin alveolar processes,
which are not used in mastication with sufficient force to carry
the blood for the nourishment of the tissues. The teeth are
changing their shape, causing the roots to come closer together,
and thus lessening the area of the alveolar process.

That the jaws of man are growing smaller is easily demon-
strated by the following procedure : Drop a perpendicular line
from the supraorbital ridge, whereupon it will be found that
the jaws of the primitive races protrude beyond the line, as is
the case with many peoples of Europe and Asia today.

Mummery, on examination of the skulls of two hundred
Britons and Roman soldiers in Hythe Church, Kent, Eng-
land, found the narrowest width 2.12 inches, the highest 2.62,
with an average of 2.50. The width of jaws of 402 British
soldiers today is : narrowest 1.88 ; widest 2.63, average 2.28.

TRANSITORY STRUCTURES. 21

The highest width was very rare, only eight measured '2.~>0.
The jaws of the mound-builders compared with the existing cliff-
dwellers show similar results, the average width is about 2.50
inches. Measurements of normal jaws of 855 Italians of Cen-
tral Italy were: narrowest 1.88, widest 2.63, average 2. 17.
Measurements of normal jaws of 1,935 Americans gave the fol-
lowing results: narrowest 1.75, widest (only one case) 2.56, aver-
age 2.13. While in the highest type of primitive man. the
width of the upper jaw from the outer surfaces of the first per-
manent molars near the margin of the gum was 2.50 inches in
diameter, the jaws of people now living in the same locality are
from 0.25 to 0.33 of an inch smaller. The antero-posterior
diameter has also shortened from one-half to five-eighths of an
inch.

Standing on the corner of Picadilly Circus and Regent
street, London, in the fall of L s< .'7. I examined the facts of
10,000 passers-by and found that eighty-three per cent possessed
jaws inside of the perpendicular line. Of 3,000 English school
children under ten years of age ninety-three per cent possessed
jaws inside of the perpendicular line, thus showing a difference
of ten per cent in one generation.

The negroes were formerly, in the opinion of anthropologists.
in the main a long-headed dolichocephalic race with protruding-
jaws. Of the Northern negroes, who in the main have white
blood, very few have long heads. The same is true of the rela-
tions of the jaws. The protrusion of the jaws has largely dis-
appeared.

That the jaw is becoming smaller is further shown by the
disappearance of the third molar, or the irregularities resultant
on its eruption because of want of room, or its eruption with
pain for like reason. In the primitive races it is large and
well developed.

THE ALVEOLAE PROCESS.

The alveolar processes are situated upon the superior border
of the inferior maxilla and upon the inferior border of the
superior maxilla. These bones, considered a part of the maxillary
bones often so described by anatomists, should, however, be con-
sidered as practically distinct bones — their structure, functions

22 INTERSTITIAL GINGIVITIS.

and embryology differ so completely from the structure and
functions of the maxillary bones. The superior and inferior
maxillae are (unlike the alveolar processes) composed of hard,
compact bone structure. The large, powerful muscles attached
to them indicate that powerful work is to be accomplished.
When fully developed they retain their full size through life.
The alveolar processes are composed of soft, spongy bone of a
cancelloid structure. As early as the eleventh week of intra-
uterine life, calcification of the deciduous teeth commences, and
by the twentieth week calcific material is abundantly deposited.
Ossification is also rapidly progressing about the dental follicles.
At birth, the sacs are nearly or quite inclosed in their soft, bony
crypts, and the crowns of the teeth upon their outer surface are
composed of enamel, which is dense and hard. The embryologic
phases of the dental shelf elsewhere cited indicate this develop-
ment.

The alveolar process, being soft and spongy, molds itself
about the sacs containing the crowns of the teeth and about their
roots after their eruption, regardless of their position in the jaw.
While the alveolar processes have grown rapidly, they have up
to this time developed only sufficiently to cover and protect the
follicles while calcification proceeds. When the crowns have
become calcified and the roots have begun to take in their calcific
material, absorption of the borders of the processes takes place in
the order of the eruption of the teeth. When the teeth have
erupted, the alveolar process develops downward and upward
with the teeth until they attain the depth of the roots of the
teeth, which extend in most instances into the maxillary bones in
the anterior part of the mouth at least, and the upper and lower
teeth rest at a point in harmony with the rami. The depth at
which they penetrate the bone differs in different mouths. This
depends upon the length of the roots and the alveolar process.
This in turn depends upon the length of the rami. The incisive
fossa, the canine eminence and the canine fossa give evidence of
this externally. These sockets are lined with extensions of the
process, thus making its upper border irregular. The crypts of
the permanent teeth are located at the apices of the roots of the
temporary teeth. The permanent teeth have large crowns which
touch each other, forming a line to the posterior part of the jaw.

TRANSITORY STRUCTURES. 23

These teeth, as they erupt, entirely absorb the alveolar process
which surrounded the temporary teeth, and as the new set conies
into place a new process is built up around them for their sup-
port. The permanent teeth require a deeper alveolar process to
support their roots, which are much longer than those of the
temporary teeth. Hence the difference in the depth of the vault
of the first and second sets of teeth.

The alveolar process of each superior maxilla includes the
tuberosity, and extends as far forward as the median line of the
bone, where it articulates with the process upon the opposite side.
It is narrow in front, and gradually enlarges until it reaches the
tuberosity, where it becomes rounded.

The process is composed of two plates of bones, an outer and
an inner, which are united at intervals by septa of cancellous
tissue. These form the alveoli for the reception of the roots of
the teeth. In some cases the buccal and labial surfaces of the
roots of healthy teeth extend nearly or quite through the outer
bony plate and are covered by the peridental and mucous mem-
branes only.

This plate is continuous with the facial and zygomatic surfaces
of the maxillary bone. The inner plate is thicker and stronger
than the outer, and is fortified by the palate bones. The external
plate is irregular upon the outer surface, prominent over the roots
of the teeth, and depressed between the roots or interspaces.

With the change in the size of jaws there is also change in
the shape of the vault and alveolar processes. When the dental
arches are large, measuring from 2.25 to 2.50 inches, the vaults
are low and the alveolar processes are short and thick, not only
giving stability to the teeth, but also plenty of nourishment.
Now that the dental arches are growing smaller, with an average
of from 1.90 to 2.00 inches, the vaults are higher in proportion,
the alveolar processes long and thin. This renders the teeth and
jaws more susceptible to trophic changes and hence to disease.
The alveolar process in the anterior part of the mouth, in which
the incisors and cuspids are situated, is much thinner than in the
posterior parts.

The sockets for the incisors and cuspids are conical and much
larger than any of the other single sockets. The alveolar pro-
cess is longer and thinner than at any of the other teeth. The

24 INTERSTITIAL GINGIVITIS.

sockets for the bicuspids are flattened upon their anterior and
posterior surfaces, and near the apices they are frequently bifur-
cated. The sockets of the molars are large at the openings.
About the middle of their length, however, they are divided into
three smaller sockets for the reception of the roots. In the case
of the third molar the number of sockets ranges from one
large cavity to three or four of smaller size. When disease
attacks the tissues, destruction is, therefore, more rapid in its
progress in the anterior parts of the mouth than in the posterior,
where the processes are thicker and more nourishment is
required.

The septa are very thin at the margin and gradually increase
in width to the middle of the jaw, where they become thicker,
and are finally lost in the substance of the jaw. Some septa are
thicker than others, and where two teeth are widely sepa-
rated, the width of the septa naturally corresponds to the space
between the teeth.

What is true in regard to a change in the size of the jaws is
also true in respect to the shape of the crowns of the teeth.
While they are not growing smaller in j>roportion to the size of
the jaws, they are changing shapes. Once they were quite well-
shaped, giving considerable space between the roots for a thick
alveolar process, thus rendering support to the peridental and
mucous membranes, now the shape has changed. The proximal
surfaces are almost straight, lessening the width and thus allow-
ing only for a thin septum, with barely sufficient surface to support
the tissues.

The sockets are lined with a thin plate of compact, bony sub-
stance, extending from the outer and inner plates of the alveolar
process to the apex, where there are small openings for the
entrance of the nerve and blood vessels for the nourishment of
the teeth.

The bony plate lias upon its inner surface the elastic periden-
tal membrane, which acts as a cushion for the teeth, while it is
surrounded by a spongy bone.

The teeth are held firmly in their alveolar sockets by the rjeri-
dental membrane. Teeth with one conical root, and those with
two or more perpendicular roots, are retained in position by an
exact adaptation of the tissues. Teeth having more than one

TRANSITORY STRUCTURES. Z>>

root and those bent or irregular, receive support from all sides
by reason of their irregularity. Fig. 5 (a section of the jaw of a
eat) illustrates the relative position of the teeth, peridental mem-
brane and alveolar process to each other.

After the removal of the permanent teeth the alveolar process
is entirely absorbed. Fig. 6 shows how the absorption takes
place. The teeth have all been removed from the superior max-
illa and the alveolar process has been entirely absorbed. The

Fig. 5.— Ground Section of Jaw and Teeth of Cat. (Andrews.)

molars on the lower jaw having been extracted, absorption of
the alveolar process has resulted in marked contrast with the
anterior alveolar process, which remains intact and holds the teeth
firmly in place. It is, hence, evident from the changes which
occur, from the first development of the teeth to their final
extraction, that the alveolar process exists solely to protect the
teeth in their crypts during development and after eruption.
After the temporary teeth are in place the alveolar process;
remains unchanged (except by gradual enlargement in harmony
with the growth of the maxillary bones) until about the sixth
year, when the second set appears. The crowns of the perma-

INTERSTITIAL GINGIVITIS.

nent teeth require more space than those of the temporary set ;
and the alveolar process must necessarily enlarge to accom-
modate them. This enlargement of the alveolar process is
caused chiefly by formation of the crowns of the permanent
teeth before eruption, and to a limited extent only by growth of

the maxillary bones. These may cease development at any
period of the life of the individual, or continue as late as the
thirty-sixth year. As diameter of the crowns of the permanent
teeth form a larger circle than that of the maxillary bones, the

alveolar process must necessarily increase its diameter and pre-
sent large spaces between the roots of the teeth for the devel-
opment of the alveolar process.

The process is solely for retaining the teeth, and if for any
reason the dental follicles should not be present, and the tooth

TRANSITORY STRUCTURES. 27

should not erupt, or if it should be extracted early, the process
would not be developed at that point. In my collection of
models are cases of arrested development of the alveolar process,
caused by the lack of bicuspid and lateral incisor germs, and by
extraction of deciduous and permanent teeth.

If one or more teeth were not to antagonize, the alveolar
process would extend beyond the natural border, carrying the
teeth with it. A marked illustration of this is seen where the
molars are decayed to the gum and the roots remain. The vas-
cularity of the process may be such that hypertrophy results.
Excessive development of the alveolar process is frequently
observed by every practitioner in connection with the anterior
inferior teeth. When the articulation is normal, occlusion of
these teeth never takes place. Frequently (especially in patients
from six to twelve years of age) these teeth extend to and
occlude with the mucous membrane of the hard palate. Such a
case is illustrated in Fig. 7. This model is taken from the jaw
of a person thirty-seven years of age, but this excessive develop-
ment took place between the ages of six and twelve years, since
at that period the vascularity of the tissues is more vigorous, and
the development of the process more formative than at any
period subsequent to the development of the first permanent
teeth.

In one case under, observation the incisors and cuspids,
together with their alveolar process, are situated upon the
external surface, while the biscupids, molars and their alveolar
process are located upon the inner border of the jaw. In
another case, the alveolar process failed to cover the roots of the
biscuspids and molars upon the outer surface, the teeth having
forced themselves into a larger circle through the alveolar process
by the contact of the crowns. The roots in this case can easily
be outlined by the finger through the mucous membrane, the
outer plate of the alveolar process barely, if at all, covering them.
Tomes 1 illustrates a case of faulty development of the outer
plate of the alveolar process, exposing the crown of the tem-
porary teeth. This occurred in a hydrocephalic. I have a
number of models showing the anterior alveolar process project-
ing beyond the normal position through the forward movement

1 Dental Surgery, page 44.

28 INTERSTITIAL GINGIVITIS.

of the molars. This may be due to a natural movement of the
molars forward, or the process may be forced forward by the
improper occlusion of the jaws. The teeth are moved from one
position to another simply by the force consequent upon absorp-
tion and deposition of bone. This is noticeable in the sjmces
between the centrals, when the alveolar process develops to a
larger circle than is necessary to accommodate the teeth. The
alveolar processes are influenced in one direction or the other by
the pressure of articulation. This results from inharmonious
development of the jaws. The teeth may come together in such
a manner as to throw the alveolar processes either to the right or
the left, thus producing a full, round arch upon one side of the
jaws, and a perfectly flat or straight arch upon the other. Occa-
sionally both upper and lower alveolar processes are carried for-
ward in the same manner. The alveolar process upon the lower
jaw is more liable to be found upon the inner border of the jaw
than is the upper alveolar process, as the inferior maxilla is
larger and more dense than the superior, and when the teeth are
once in position upon the lower jaw they are not so liable to
subsequent change. Owing to this the teeth of the superior
maxilla do not form so great a circle. This causes the teeth
upon the sides of the jaw to conflict, and the lower teeth and
alveolar processes to be carried in, while the anterior teeth of the
lower jaw are held inside of the superior anterior teeth, thus car-
rying the alveolar processes inward.

The teeth are continually changing their positions in the
mouth. This is as often beneficial as it is detrimental. That the
teeth may perform their full function, they should not only
remain firmly in the alveolar process, but they should also antag-
onize properly. The teeth may be compared to the bricks in an
arch. Remove a brick and the arch falls to pieces. It is fre-
quently found that the teeth do not articulate properly ; by a
slight movement, or by cutting away the grinding surfaces, a
better articulation may be secured. When this operation is per-
formed, the teeth move in their sockets by absorption and depo-
sition of bone, demonstrating the fact that the process changes in
shape and substance. Ziegler 1 says absence of functional use is
a, frequent cause of premature lacunar absolution of the bone.

1 A Text-Book of Sj^ecial Pathological Anatomy, page 145.

TRANSITORY STRUCTURES. 29

This form of atrophy from disuse occurs not only when a limb or
a part of a limb is deprived of its normal activity, but also when
portions of a single hone cease to perform their function of sup-
port, and finally, like all the hones of the body, as age advances.
normal or physiologic absorption takes place, while the teeth are
still in the jaws. Unlike other bones of the body, however, the
absorption of the alveolus progresses to a greater extent because
of the unstable condition of the structures.

From what has already been said of the vascularity of the
alveolar process, it is evident that hypertrophy of the tissue may

ensue from an unbalanced nervous system and from simple irri-
tation of varying degree. The irritation consequent upon the
eruption of the teeth, together with the excessive blood supply,
are both primal causes of overbuilding of tissue, i. e., hyperplasia.

The ragged roots of the temporary teeth, produced by absorp-
tion of the gases from the putrescent pulps, and the pressure of
the permanent crowns against the tissues, produce sufficient
stimulation to excite physiological action. Tissue-building gener-
ally is seen in connection with all the teeth, and the process
becomes unnaturally thick, the teeth frequently are carried in
one direction and another; cementosis of the roots of the teeth
and hypertrophy of the process result.

In cases of hypertrophy of the alveolar process, enlargement
is associated with the inner plate of the alveolar process. In
cases coming under my observation the inner plate in most is the

30 INTERSTITIAL GINGIVITIS.

part of the alveolar process affected (Fig. 8 case). The outer
plate, although quite irregular from the arrangement of the teeth,
is usually normal in thickness. This disparity in the two plates
of the alveolar process is clue to the fact that the inner plate of
the alveolar process possesses a large blood supply, the posterior
or descending palatine arteries furnishing the ossific material. I
have observed but few cases where hypertrophy has extended to
and included the outer plate. When the outer plate becomes
involved the alveolar process assumes a very thick condition.
Occasionally hypertrophy will affect one side only or one distinct

locality (Fig. 9). In this case the enlargement is upon the left
side and extends from the first bicuspid posterior to and including
the maxillary tuberosity. Instead of the force being directed
inward, as is generally the case, the process is forced outward and
backward. This enlargement occurred previously to the develop-
ment of the second and third molars. The alveolar process
extends downward and occludes with the teeth upon the lower
jaw, thus preventing the molars from erupting.

Under the microscope, two systems of Haversian canals are
seen in the alveolar process. Kolliker 1 describes these as follows :

"The Haversian canals are of two kinds. One with the
regular lamella? system surrounding it, and the other, the so-called

1 Handbuch der Gewebelehre, page 272.

TRANSITORY STRUCTURES. 31

Volkmann's canals, containing the perforating vessels from Yon
Ebner, which have no surrounding lamellae, but simply penetrate
through the layers of bone. Volkmann's canals are present in
all tubular bones in old and young. While especially present in
the outer basal lamellae, they occur also in the interstitial leaflets
and in the inner chief lamellae as well as in the periosteal layers
of the skull bone. Here their number is very variable (Fig. 10).
They run partly transversely or obliquely, and also partly longi-
tudinally, through the lamellae. Many of these canals open in

Fig. 10. — Section of Bone Showing Blood Vessels of Von Ebner.

the outer or inner surfaces of the substantia (compact substance),
and also here and there in the Haversian canals, and form alto-
gether usually a wide-meshed irregular network. In their struc-
ture they are sometimes smooth and sometimes furnished with
dilatations and angles projecting in and out in profile. The
widest has a diameter of 100 micrometers or more, and the
narrowest not more than 10 or 20 micrometers, and there are still
narrower ones which are altogether obliterated, appearing like
rings or circular-formed structures without any lumen, or like
those far from rare obliterated true Haversian canals first
described by Tomes and de Morgan. The contents of the
Yolkmann canals are the same as the Haversian canals."

Fig. 1() is a cross section of the medulla of a calcined human

INTERSTITIAL GINGIVITIS.

"humerus slightly enlarged. The outer lamellae contains a large
number of Volkmann's canals running longitudinally and trans-
versely and extending through the outer plate of bone into the
periosteum. Fig. 11, the cross section of the section seen in
"Fig. 10, shows these canals more highly magnified. The Haver-
sian canals are large round spaces (Fig. 12), containing a single
artery and vein. The fine hair-like spaces running from these
large spaces are the canaliculi. The dark spots circulating each
Haversian canal are the lacuna?. The canaliculi run from one
lacunae to another or into a Haversian canal or they anastomose
-with each other. The rings of bone about each Haversian canal
.are called lamellae. The lacunas seem to be about uniformly

: - r ---2rc e°

Fig. 11.— Section of Bone (Higher Magnification) Showinq Blood Vessels of
Von Ebnkr.

■distributed throughout the bone. The spaces between the
lacunae and canaliculi are filled with lime salts.

A longitudinal section of bone (Fig. 13) is similar in appear-
ance to the cross section. Instead of the lacunae being arranged
in rows around the Haversian canals they are parallel. It will
be noticed that the Haversian canals run in different directions
and communicate with each other at certain intervals. The

TRANSITORY STRUCTURES. 33

foregoing description, with illustrations from Kolliker, is essen-
tially that of the minute anatomy of the alveolar process.

THE PERIOSTEUM -VXD PERIDENTAL MEMBRANE.

The periosteum is a fibrous tissue covering the outer surface
of the alveolus. The peridental membrane is composed of
similar structures covering the roots of the teeth and lining

-^SBfejl * '»

Tig. 12. — Transverse Section of the Diaphysis of the Humerus Magnified 350

Times.

a, Haversian Canal. Dark spaces, Lacunar. Hair-like spaces, Canaliculi.

the inner wall of the alveolus. They are both derived from
the mesoblastic layer. For this reason there can be very little
difference in the character of the structure of each, except so far
as function is concerned. The periosteum is made up of four
different kinds of fibers. An outer layer of coarse, white fibrous
tissue, an inner layer of fine, white fibrous tissue, elastic fibers,
and penetrating fibers (fibers of Sharpey).

The fibers of the periosteum are coarser than those of the
peridental membrane. The coarser fibers run parallel with the

INTERSTITIAL GINGIVITIS.

alveolar process (J) over the border and extend as far as the
union of the epithelial layer (E) and the periosteum (H), Fig.
14. ("The dental ligament," Black. 1 ) The finer fibers run in
all directions and enter the alveolar process at every point. If a
section of the alveolar process treated with acids or a section
affected by halisteresis or osteomalacia be placed under the
microscope, the fibers are seen to retain the original shape of
the bone.

The fibers of the periosteum, therefore, are continued
throughout the process from the periosteum on the one side

fob I0m,i!

Fig. 13. — Longitudinal Section of Bone Magnified 100 Times.
a, Haversian Canals. 6, Lacunae seen from the side, c, Canaliculi.

to the peridental membrane on the other. This is also illus-
trated in the mouths of persons, where (after wearing artificial
dentures for a short time) heat produces absorption of the lime
salts, leaving the fibrous tissues intact.

The periosteum is abundantly supplied with blood vessels
which anastomose with each other and enter the alveolar process,
at the Haversian canals. The plexus of blood vessels is much

1 American System of Dentistry, page 663.

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third.

Fig. 14. — Longitcdinal Section of Tooth, Alveolar Process, Peridental Membrane ani
Periosteum. Normal Tissue. Sheep.

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane.
H, Periosteum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, Fibrous
Tissue. AA, Point of union of epithelial tissue and peridental membrane.

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third.

Fig. 15. — Cross Section of Tooth, Alveolae Process, Peridental Membrane and
Periosteum. Normal Tissue. Dog.

B, Dentine. C, Cementum. D, Pulp. H, Periosteum. J, Alveolar Process.
K, Capillaries. M, Fibrous Tissue. U, Nerve Tissue. C T, Connective Tissue.

TRANSITORY STRUCTURES. 37

larger proportionately in connection with the alveolar process
than with other bones of the body, owing to its transitory
nature.

The peridental membrane commences at the margin of the
epithelium at the neck of the tooth AA, Fig. 14, and is attached
directly to the cementum. This membrane has various func-
tions: First, it fills the space between these two structures,
forming a cushion for the teeth to rest upon ; second, like the
alveolar process, it is present only when the teeth are present,
and therefore develops with the alveolar process when the first
teeth erupt, it is entirely lost when the temporary teeth are shed,
is restored with the eruption of the second set, and when the per-
manent teeth are extracted it disappears with the alveolar process
completely; third, it furnishes the nourishment for the teeth
while they are in position in the jaw, and holds them in their
sockets.

The fibrous tissue, in its earliest stages comprises nearly all
or quite all of that portion of the jaw which eventually becomes
the alveolar process. Calcification begins at the center of the
jaws and gradually closes in upon the fibrous membrane until it
becomes the thickness of a sheet of paper. In young persons
the membrane is much thicker than in old age, since, as age
advances, the osteoblasts on the one hand and the cementoblasts
on the other send out new material and each wall closes in upon
the membrane, which becomes very thin in old age and almost lost.

The fibers which compose this membrane extend in all direc-
tions ; some crosswise penetrating the cementum, on the one
hand, and the alveolar process on the other. In a general way,
since the fibers extend through the alveolar wall, they are more
closely adherent to the bone than to the cementum, and usually
cling to the latter when the tooth is removed. It will be observed
that these fibers do not enter the alveolar process uniformly as
claimed by Gray 1 and Pierce 2 , like tacks or nails driven regularly
into a board (the "fibers of Sharpey " Fig. 14), but vary as to
quantity in different localities. In some localities they penetrate
in large quantities and almost surround a piece of alveolar pro-
cess, while a few fibers penetrate but a short distance. In some

Anatomy.

American System of Dentistry, page i

38 INTERSTITIAL GINGIVITIS.

places, the) 7 can be traced almost through the alveolar process.
These fibers are much finer in man (Fig. 15) than in the lower
animals (Fig. 14, dog). In connection with the fibers which pass
into the alveolar process are numerous blood vessels. Others run
diagonally, and still others lengthwise, all making up a tissue
which holds the tooth in position in the jaw. The fibers enter
the peridental membrane at all points of the process, from its
margin to the apex of the roots. The elasticity of this membrane
is so great that in correcting irregularities a tooth may be turned
from one-fourth to one-half around without breaking the fibers.
The elasticity is greatest in youth. As age advances, the mem-
brane grows thinner and thinner until, late in life, there is almost
a bony union between the tooth and the alveolar process, thus
preventing stretching of the fibers. At the upper border, under
the gum tissue, these filters extend over the edge of the alveolar
border and unite with the fibers of the periosteum on the outer
border of the process, forming the interstitial tissue.

If absorption of the inorganic substance of the alveolar pro-
cess occurs, the fibrous tissue retains the shape of the process.
The same results when inflammation of the peridental membrane
takes place at the gum margin or at the apex of the root of the
tooth. What was once alveolar process is now peridental mem-
brane or fibrous tissue.

Two kinds of structures are present in the alveolar process —
a dense, compact, hard structure (composed of lime salts), and a
fibrous tissue ; either alone will retain the shape of the tissue.

Blood vessels permeate this membrane throughout from the
gum tissue at the neck of the tooth, through the alveolar walls
to the end of the roots. They are most abundant in youth.
Capillary blood vessels enter the Haversian canals through the
process and into the cementum. Many of these blood vessels
extend the entire length from the gum margin to the apex in
straight lines and vice versa, In many of the illustrations, the
blood vessels will be seen to follow the line of the alveolar pro-
cess (Fig. 14). A great supply of blood vessels penetrate the
membrane through the alveolar walls. These vessels unite and
anastomose with the arteries which traverse lengthwise, forming
a complicated plexus (Fig. 16). According to some writers the
vascular supply of the peridental membrane is situated in the

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third.

Fig. 16.— Cross Section of Tooth, Alveolar Process and Peridental Membrane.
Injected Blood Vessels. Normal. Doc

B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. K, Capillaries.
L, Haversian Canals.

Micro-photographs, reduced one-third.

Fig. 17.-Ce
B, Dentine. C, Cementum

Section of Tooth, Alveolar Process and Peridental Membrane.
Injected Blood Vessels. Normal. Dog.

I, Peridental Membrane. J, Alveolar Process. K, Capillaries.
L, Haversian Canals.

TRANSITORY STRUCTURES. 41

center of the structure. This has not been my experience. All
of my slides, as well as those here presented, show the blood
vessels to be situated nearest the alveolar process. It is quite
natural that this should be so, since very little blood is required
for the nourishment of the cementum, while the largest amount
is required to supply the alveolar process. The system of blood
vessels situated in the peridental membrane and showing their
relation to the surrounding tissue is well shown in the injected
specimen from healthy dogs (Figs. 16 and 17). Pus pockets and
abscesses are hence more liable to form near and in the alveolar
process than near the tooth structure. When infection takes
place, the products of inflammation are carried through the
blood vessels and the foci of round cell inflammation are located
near or in the alveolar process where abscesses form. The vessels
seen in the membrane anastomose very freely with those at the
gum margin, showing the membrane to be well nourished in all
its parts. Should one part become involved by disease the other
parts are overnourished in consequence.

These blood vessels enter the alveolar walls with the fibrous
tissue through the Haversian canals and these in turn permeate
the entire bone. As age advances, however, the bone becomes
more dense, and the Haversian canals become smaller and (under
certain conditions) cease to exist. When disease takes place,
either at the gingivus or at the apex of the root, the supply of
blood being thus cut off, the tissues receive sufficient nourishment
through the alveolar wall. Since the structures are in a transi-
tory state, being destroyed and repaired so frequently, it is evi-
dent why the blood supply is so rich.

CALCOSPHEKITES.

Small, hard bodies are frequently found in the peridental
membrane. These are sometimes in the form of concentric rings
of lime salts and are called calcospherites. They are not always
round, but may be of any shape and vary as well in size. They
bear the same relation to the peridental membrane that pulp
stones do to the dental pulp. Black 1 says: " I have seen more of
them about the roots of the molars than elsewhere, but have
found them along the sides of the roots of the bicuspids."'

1 Periosteum and Peridental Membrane, Page 94.

42 INTERSTITIAL GINGIVITIS.

When irritation and inflammation take place in the peridental
membrane, the cementoblasts build up cement substance, just as
the osteoblasts do in the alveolar process and the odontoblasts do
in the pulp chamber. Sometimes they are attached to the root
of the tooth, which produces what is called exostosis or cemen-
tosis. They may remain unattached, floating in the fibrous tissue.
These are very common in connection with interstitial gingivitis.

GUMS AND MUCOUS MEMBRANE.

The tooth, according to Minot, 1 is a papilla which projects
into the epidermis, and ossifying in a particular way, changes into
ivory around the soft core or pulp. To the papilla the e]:>idermis
adds a layer of enamel. The tooth proper unites with a small
plate of dermal bone at its base. By a modification on the jaw,
the epidermis first grows into the dermis, and then the dermal
tooth papilla is developed. The teeth were primitively organs of
the skin and widely developed over the surfaces of the body. As
the mucous membrane is practically a continuation of the skin, it,
in accordance with the law of individuation, became specialized
and lost some of the functions of the skin while developing the
others to greater j)erfection.

The mucous membrane lines the cavity of the mouth, the
nose, and extends through the larynx into the lungs and through
the oesophagus into the stomach. It covers the tongue, jaws,
alveolar process, dipping down between the necks of the teeth
and the alveolar process as far as the peridental membrane, leav-
ing a free space between the membrane and the teeth through its
entire length.

It consists of two layers (Fig. 18), the epithelium (A) and
corium (B), separated by the basement membrane (C). The
epithelium is composed of the epithelial cells : First, one row of
columnar cells (B) situated upon the basement membrane (C);
second, two rows of six-sided prickle shells (E); third, two rows
of six-sided cells (F); fourth, two or three rows of squamous
cells (G) ; and fifth, four or five rows of flattened dead cells (H),
which were originally the columnar cells upon the basement
membrane. The young new cells are the columnar cells which
pass from one stage to another, changing their shapes until they

1 Embryology, page 481.

TRANSITORY STRUCTURES.

eventually become dead cells and are exfoliated from the surface
of the tissue. The basement membrane (C ) is made up of fibers
running longitudinally, from papillae, which allow the tunica
propria containing blood vessels and nerves to pass up into the
epithelium structure.

The corium (B) (which lies below the basement membrane )
is composed of alveolar connective tissue, white yellow fibrous
connective tissue, muscular fibers, nerves, blood vessels and
lymphatics. It is made up of the tunica propria and the
submucosa.

Fig. 18. — Diagrammatic Illustration of the Epithelium and Submucous Layers or the
Mi cous Membrane.
A, Epithelium. B, Corium. C, Basement Membrane. D, Columna Cells. E, Prickle
Cells. F~ Six-sided Cells. G, Squamous Cells. H, Flattened Dead Cells.

The tunica propria (beautifully shown in Fig. 1 ( .») con>i~t~
of interlacing connecting fibers interspersed with much elastic
fibrous tissue. This tissue penetrates the epithelial layer in the

44 INTERSTITIAL GINGIVITIS.

form of cone-shaped papilla;, varying in length with the thick-
ness of the epithelium. This layer being the thickest at the
gum margin (E), these papillae are the longest and largest at this
locality. The fibers of the tunica propria pass gradually into
the submucous membrane (G), and from there into the perios-
teum and peridental membrane (M), so that it is difficult to
determine the mucous capacity line of demarcation separating the
different structures. The submucosa is composed of fibrous
connective tissue of a much less compact variety. This structure
is attached to the bones through the periosteum and peridental
membrane. In this structure the glands, blood vessels, nerves,
fat cells, etc., occur.

The larger blood vessels (K) are found in this structure.
From these large blood vessels small capillaries extend to the
tunica propria. It is here that inflammation commences in
interstitial gingivitis. Numerous veins accompany each artery,
and lymphatics form a network around them. Small nerve
filaments are also in this structure, which pass through the tunica
propria and into each papilla in connection with the capillaries.
The terminal nerve fibers come in contact with the muscular
fibers, so that there is direct communication by blood vessel and
nerve throughout the mucous membrane from the nose, stomach
and lungs. The gum tissue is very thick and made up of fibrous
tissue running in three or four directions, rendering it dense,
tough and hard. The membrane thus differs from the same
structure in other parts of the body. On account of these
numerous fibers, this structure is bound tightly to the alveolar
j)rocess. The gum tissue acts as a cushion and protection from
irritation which may arise from hard substances being taken into
the mouth. As this membrane passes and coalesces with the
membrane of the lips and cheeks, it becomes much thinner and
less dense. In the center of the tooth, the parallel fibers in the
tunica propria are composed of flattened fasciculi of connective
tissue. There are three sets of fibers — those which run verti-
cally, those which radiate and are fan-shaped, and those which
are horizontal.

The mucous membrane, like the alveolar process and peri-
dental membrane, is composed of very unstable tissue. It
changes its structure, blood vessels and nerve system as often

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third.
Fig. 19. — Longitudinal Section of Tooth and Gum Tissue.

Dog.

D, Dentine. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. M, Fibrous
Tissue. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peridental
Membrane. RR, Space Pocket from Want of Union of the Epithelial Fold.

46 INTERSTITIAL GINGIVITIS.

as the other structures. Its blood vessels and nerve system are
continually renewing connective tissue, periosteum and peridental
membrane.

A difference is noticed in the structure of the papillary layer
in man and the lower animals, such as the dog, the sheep and
the calf. In man the gum tissue is not so thick, therefore the
papilla? are broader and shorter, while in the loAver animals the
papillae are narrow, long and more closely set together. Blood
vessels and nerves are not so numerous and close together in man
as in animals.

DO GLANDS EXIST IN THE MUCOUS AND PERIDENTAL
MEMBRANES ?

A somewhat widespread opinion locates special glands in the
gingival tissues and the peridental membrane. This seems, to a
certain extent, to be in part due to the lack of definite knowl-
edge as to the etiology of interstitial gingivitis, and in part to the
fact that certain constitutional conditions, such as mercurial and
potassium iodide poisoning and scurvy, manifest themselves in
the gum tissue in a way similarly to their action in the glandular
structures of the body. Black 1 claims, for example : " That part
of the gingival margin that lies in against the neck of the tooth
is of a different structure from its other parts. Here it is clothed
with a very soft, round or polygonal gland-like epithelium that
suggests the formation of a gland, but fails to assume the
glandular structure, though it seems to have been regarded as
such by Serres. This — which I shall call the gingival organ —
emits a profusion of small rounded cells which are always found
in the saliva (Salter) and are usually called mucous-corpuscles.
It is well known that certain glands have the power of the selec-
tion and excretion of certain j)oisons, and in this way of elimi-
nating them from the system, and that if the substance be in
large amount, hyperemia, or even inflammation, may result. It
is also known that mercury and potassium iodide will produce
inflammation of the free margins of the gums, and Salter has
found that these cells are in greater abundance under these cir-
cumstances ; also that the cells taken from the gingival border

American System of Dentistry, pages 955-956.

Fig. 20.-

>. A. A. obj. Zeiss. Micro-photographs, reduced one-third.
-Longitudinal Section of Gum. Normal Tissue. Sheep.

C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries.
M, Fibrous Tissue. AA, Point of T'nion of Epithelial Tissue and Peridental Membrane.
Nm, Naysmith's Membrane. Sg, So-called Glands of Serres.

48 INTERSTITIAL GINGIVITIS.

and submitted to chemical tests after the person has taken potas-
sium iodide, are found to yield, and are tinged with, iodin."

Longitudinal sections of the tooth, alveolus and surrounding
tissues, under the microscope, exhibit a very peculiar formation
of the mucous membrane at its line of union with the peri-
dental membrane at the neck of the tooth. Black ' (in an
article beautifully illustrated by Frederick Noyes) seems to
identify these with the so-called glands of Serres, or gingival
glands (Fig. 20). He speaks of them as glands in various
places throughout the article ; for example, " But little can now
be said of the function of the network of glands of the periden-
tal membrane, beyond what is indicated by their form, location
and histological characters. With the knowledge of their posi-
tion and general character, clinical observation leads to the con-
clusion that they are readily disturbed by certain drugs, notably
by mercury and iodin ; and that they are often disturbed by
.substances poisonous to them floating in the blood streams. This
is evidenced by the appearance of marginal gingivitis, with
soreness of the peridental membrane. Such disturbances would
not be likely to occur without the presence of some specialized or
secretory tissue. ... It seems to me very certain that the
disease which I have described as phagedenic 2>ericementitis has
its seat' in these glands." Black, however, does not seem quite
certain of the validity of his position, since he further remarks,
" Though definitely lobulated, this body does not seem to jwssess
the characters of a gland, and I should not suppose from an
examination of its tissues that it had a glandular function. It
encircles but a portion of the neck of the tooth, usually only the
approximal portion, thinning away toward the buccal and
lingual, so that in many of the lengthwise sections it may be
very small, or does not appear at all."

In many slides of sections from canine jaws and human, 2 the
same peculiar arrangement of structure was observed, although
not in so marked a degree. In the immature herbivora (calf and

1 Dental Cosmos, February, 1899.

2 The material obtained for making slides from man, other than the scurvy cases,
■was obtained through the kindness of surgeons from jaws removed from hospital
patients, as a result of disease ; the surgeons placing them into alcohol or Muller's
solution as soon as removed.

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third.

Fig. 21. — Cross Section of Tooth and Peridental Membrane. Normal Tissue. Sheep.

C, Cementuni. D, Dentine. I, Peridental Membrane. W, Epithelial Debris

X 300. No. 2 projection ocular. D. D. obj. Zeiss. Micro-photographs, reduced one-third.
Fig. 22. — Cross Section of Tooth and Peridental Membrane. Normal Tissue. Shi
C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris.

TRANSITORY STRUCTURES. 51

Lamb) these peculiar formations of structure art' well marked,
albeit less so in the carnivora, and still less in man.

Were glands present in this locality it is logical to infer that
they would become involved in mereurialism, plumbism and
scurvy, and exhibit marked inflammation with broken-down
structures in a given locality, as at the union of the gum tissue
with the peridental membrane. Such a case is unknown.

The mucous membrane tinder the microscope appears at a
point between the teeth (and faintly so at the inner and outer
border as shown by Black) to double upon itself. When the
tooth erupts, absorption of the gums occurs at the highest point.
The gum tissue passing down to the neck of the tooth folds or
crowds upon itself between the teeth with a peculiar curve
downward, inward and then outward and upward. At the
upper border, about midway from the gingival margin to the
neck of the tooth, may be seen a space or pocket (never twice
alike in appearance) where the edge of the gum tissue comes in
contact with the original epithelium. Sometimes the space or
pocket is closed up (Figs. 43, 44, 51). Again it remains open
(Figs. 19, 32, 50, 53). Frequently this peculiar type of
structure is absent, showing that the fold of gum tissue either
has been absorbed in the eruption of the tooth or did not form.
This peculiar form encircles only a portion of the neck of the
tooth (according to Black's examination of the structure in
sheep). This in itself seems to oflsel the glandular theory, since
gingivitis almost invariably starts on the lingual or palatine and
labial surfaces where this structure does not appear. In the
slides of the scurvy case there does not appear the slightest
evidence of anything resembling glandular structure. Hence
it would seem safe to conclude that the glandular structure does
not occur in this locality. It is by no means impossible that in
the peculiar epithelium in this locality, epithelial cells undergo
changes which to some observers simulate glandular structure,
but on histologic analysis are distinguishable from it, resembling
in this the crypts of the head of the penis.

In cross sections of the peridental membrane, with a low
power may be seen dark bodies arranged along the margin of the
cementum in the peridental membrane (Fig. 21). They are
more numerous, however, near the gingival border than at the

INTERSTITIAL GINGIVITIS.

root extremity. These bodies are more numerous and better
defined in the sheep than in the calf, and more apparent in the
canine jaw than in the human. Under higher power (Fig. 22)
they may be distinctly demarcated as epithelial cells arranged

. wclfth obj. Zeis

Fin. 23. — Cross Section of Tooth and Peridental Membrane. Normal Tissue.
Sheep.

C, Cementurn. D, Dentine. I, Peridental Membrane. W, Epithelial Debris.

in single rows of loops, again in double rows, again in rows of
three and sometimes in round or oblong groups, with clusters of
cells without shape or form. With a still higher magnifying
power (Fig. 23) it will be seen that these masses of cells are
polygonous, never prismatic. They hence are similar in shape

TRANSITORY STRUCTURES. 53-

to the epithelial cells situated above the columnar cells. They
also resemble the cells which are situated inside of the epithelial
lamina. In the larger amplification the nucleus can be readily
observed.

Black 1 has attempted to demonstrate that glands exist in
the structure and that the cells last mentioned are glands.
Black lays down as a sine qua non of a gland that there should
be an opening to the surface. He has made an attempt (Fig. 15)
to demonstrate such an outlet, but this figure does not show
clearly that the glands empty into the duct or have an exit at
the surface. These bodies, however, not only fail (like the
ductless glands) in this particular, but in more important
characteristics of glands. They do not have (as Robin and
Magitot remark) a columnar or prismatic cell wall. It is not
difficult to understand how epithelial cells are scattered in dif-
ferent shapes and sizes throughout the peridental membrane.
Epithelial cells have the property of multiplying and develop-
ing in structures wherever located. 2

If epithelial cells should migrate within the submucous mem-
brane and fibrous tissue, proliferation will occur under certain
circumstances. The tooth, according to Minot, 3 is a papilla
which projects into the epidermis and, ossifying (calcifying) in a
particular way, changes into ivory around the soft core or pulp ;
to the papilla the epidermis adds a layer of enamel. The tooth
proper unites with a small plate of dermal bones at its base. By
a modification in the jaws the epidermis first grows into the der-
mis and then the dermal tooth papilla is developed. The first
indication of the development of tooth germs in mammals is a
thickening of the epithelium covering the jaw. This thickening,
which appears as a ridge during the sixth week of embryonic
life, forms on the under side of the epithelium. This curving
ridge expands into an outer portion (the outline of the groove
between the lip and the gum) and an inner portion, the dental
shelf which grows obliquely inward. The papillae for the milk
teeth are formed on the under side of the shelf, and it is thus
possible for the shelf to continue growing toward the lingual

1 Dental Cosmos, February, 1899, pages 112-118.
-'Dental Follicle, page 116.
•Embryology, pages 581-90.

54 INTERSTITIAL GINGIVITIS.

side, so that the second set of germs is developed for the perma-
nent teeth. The end of the shelf, toward the articulation of the
jaws, is prolonged without retaining the direct connection with
the epithelium and from this prolongation arise the enamel
organs for the three permanent molars. Wherever a tooth-germ
arises the dental shelf is locally enlarged, and the local enlarge-
ment constitutes an enamel organ which projects from the under
side of the shelf. The portions of the shelf between the enamel
organs gradually break up, forming first an irregular network,
and later separate fragments ' which may persist throughout
life and lead to various pathological structures. While the per-
manent germs are forming, the shelf is solid between them,
although it has assumed the reticulate structure between the
germs of the milk teeth. In consequence of the reticular forma-
tion, the fully developed enamel organs have several bands or
threads by which they are connected with the dental shelf proper.

After the shelf has developed somewhat, its line of connection
with the epithelium of the gum becomes marked by a superficial
groove, as may be seen in the human embryo of eight to ten
weeks. This groove was formerly supposed to be the first trace of
the dental shelf, but Rose's observations correct the supposition.

The second step in mammals is the formation of outgrowths
(in man ten in each jaw) from the under side of the dental shelf;
each outgrowth is the outline of an enamel organ for a milk
tooth. The outgrowth is covered toward the mesoderm by a layer
of the epidermis, while the core is filled with polygonal cells
which resemble those of the middle part of the Malpighian layer
of the skin. The outgrowths, after penetrating a short distance,
expand at the lower ends, but remain each connected by a nar-
row neck with the overlying ej^idermis. The expanded end is
the enamel germ proper ; it very soon assumes a triangular out-
line, as seen in sections, owing to the flattening of its under side,
and at the same time it moves somewhat toward the lips. Mean-
while the shelf continues growing on the lingual side of each
ingrowth to produce the enamel organs destined for the second
or permanent teeth.

At this stage it is noticed that the mesenchyma under the
flattened end of the enamel organ has become more dense, to

Including the epithelial debris of Robin and Magitot.

TRANSITORY STRUCTURES. 55

form the outline of the dental papilla, and is beginning to develop
fibrillse around both the enamel germ and the papillary outline.
The fibrillar envelope is the future dental follicle.

The third step is a final differentiation of the enamel organ
and the accompanying shaping of the papilla. The enamel
organ continues growing and becomes concave on its under side
.so that the mesoderm underneath acquires the shape of the
papilla. It is now that the form of the tooth is determined by
the form assumed by the papilla, which in its turn is probably
determined by the growth of the enamel organ.

The follicle is merely an envelope of connective tissue in
which can be distinguished an outer dense and inner looser
layer; in the latter the cells are more distinct and the fibrillar
are less numerous than in the former. A rich network of capil-
lary vessels is developed in the follicle and appears in part as a
series of villous-like growth into the enamel organ. The follicle
develops first over the lower part of the papilla, then over the
enamel organ, the neck of which aborts and the follicle closes
over, completely separating the enamel organ from its parent
epidermis. The enamel organ changes greatly in appearance.
The layer of cylinder cells is well preserved over the concave
surface, but only where the epithelium is in contact with the den-
tal papilla. In the neck the cells become irregular in form.
Over the convex surface the cells become lower and cuboidal.
They ultimately atrophy and flatten out. The cells in the center
of the enamel organs undergo a peculiar metamorphosis. They
remain united together by a few thread-like processes.

It is obvious from these changes in the embryo how what
Robin calls the epithelial debris is derived from the epithelial
cord, the follicular wall and the round bodies of lamina epithel-
ium debris. According to Ch. Robin and Magitot,' who were
the first to describe these • bodies, "The phenomena of budding
commences, namely, when the epithelial cord has finished its
course, having conducted the primary enamel organ to that point
whence its subsequent evolution will be effected and soon after
the formation of the secondary follicle, immediately after the
rupture of the cord of the primitive follicle." Robin leans to

'See their Memoir on the Genesis and Development of the Dental Follicle in
Jour, de Physiologic de Brown-Sequard, 1860.
5

IXTEBSTITIAL GINGIVITIS.

the opinion that these bodies disappear soon after they are
formed, " The time of their disappearance varies, they remark,
in different species of animals. In the human embryo the
remains of the cord of the primitive follicles may be found, even
after the formation of the follicles of the permanent teeth, and
it is probably during the process of eruption that these bud-
dings become atrophied ; in the canine embryo the facts are
nearly the same ; in the bovine and ovine embryos (calf and
lamb) it has seemed to us that these proliferations disappear at a

•2BI^

Fig. 24. — Section through the Incisive Portion of the Lower Jaw of an Ovine
Embryo, Measuring 82 Millim (3J Inches) in Length. Magnified 260 Diam.,
after Drs. Ch. Legros and E. Magitot.

D, Oral Epithelium. C, Lowest Layer of Cells in the Stratum Malpighii.
F, Epithelial Cord. K, Bourgeon of the Secondary Cord. I, Follicular Wall.
H, Dental Bulb.

correspondingly earlier stage ; and we think it safe to say that,
as a general rule, the complete absorption occurs toward the
j>eriod of eruption."

The embryology of the dental shelf, which has been sum-
marized by Minot from Waldeyer, Kolliker, Von Ebner 1 and
O. Hertwig, indicates the source of the structures which have
been mistaken by Black for the limiting walls of glands.

1 Handbuch der Zahnheilkunde, 1890, pages 209-262.

TRANSITORY STRUCTURES. 57

After the epithelial cords of the temporary and permanent
sets of teeth have been demarcated from their follicles, the proc-
ess of cell building proceeds like the process of cord building.
These buds, according to diaries Robin and Magitot, 1 are given
off at the upper border of the follicle and below the epithelium
of the gum. "In fact, as soon as the epithelial lamina loses its
connection with the follicle, by the rupture of the cord, the epi-
thelial cells composing it become greatly increased in number at
the severed point. The multiplication of cell-elements results

-b

Fig. 25. — Vertical Transverse Section through the Incisive Region of the
Lower .Iaw of Human Fostcs Measuring 38 Centimetres (15} Inches), Mag-
nified SO Diam., after Drs. Cii. Legros and E. Magitot.

b, Bony Formation. d, Oral Epithelium. g, Enamel Organs. H, Dental
Bulb. I, Cord of the Permanent Follicle. K, Debris on the Follicular Wall of the
Primitive Follicle and from its Cord. K, Epithelial Globule. L, Enamel Organ of
the Permanent Tooth.

in the formation of irregular buddings, which wander in different
directions into the deeper portions of the embryonal tissue.
These buddings vary greatly in form ; sometimes they are sim-
ple cylinders, retaining their connection with the primitive
lamina by pedicles of various lengths, and sometimes this slight
connective is absorbed, thus isolating an epithelial mass."

This budding occurs at different points along the cord (Fig.
24 ) at the end and upon the outer surface of the follicular wall
(Figs. 25 and 26) at the point where the cord is severed from the

^oc. cit, 1S60.

58 INTERSTITIAL GINGIVITIS.

enamel organ. These gradually diminish as they descend upon
its sides. Doubtless the epithelial cord remains in the periosteal
and submucous tissue throughout life. Fig. 27 represents evident
sections of epithelial cord in a man sixty-eight years of age, and
Fig. 28 in a dog eight years. In the photographs of the scurvy
cases and of dogs will be seen evidences of the persistence of
epithelial debris late in life. The position already cited from

'■'■';',' ■ ■-■ ■ * ■■■-■

'■ ■.' '' ."rtC'iTfiTuiroi- f) -,..„ ;.„,,,„ .-- : "'

WJo

Fig. 26. — From the Lower Jaw of ax Ovine Embryo, Magnified 80 Diameters,
Showing the Completed Dental Follicle and the Surrounding Tissues,
after Drs. Ch. Legros and E. Magitot.

a, Meckel's Cartilage. b, Traces of Ossification, c, Lowest Layer of Epithelial
Cells, d, Oral Epithelium. F, Ameloblastic Layer. F, (Lower) External Layer of
the Enamel Organ — a continuation of the Layer of Ameloblasts. g, Stellate reticu-
lum of the Enamel Organ. H, Bulb. I, Follicular Wall. K, Buddings from the
Cord.

Robin and Magitot as to its early disappearance would hence
appear to be too strongly taken.

Robin and Magitot claim that this budding process occurs at
or about the time of the rupture of the cord. Up to this period
ossification has not taken place, but then deposits of bone appear
in the fibrous tissue of the middle and outer surfaces. The bone
deposit gradually takes the form of the jaw, filling in and
encroaching upon the fibrous tissue, forming a bony wall on the

TRANSITORY STRUCTURES

one hand, and the crown and root of the tooth on the other.
When the tooth is ready to erupt, the crown pushes the soft tissue
laterally, while the root develops, forms a defined wall with the
peridental membrane between them. The epithelial debris ( to
use their term ) which before was scattered over the entire surface
of the dental follicle, is now crowded into the very narrow space

X 50. One-half-in. obj. No, Oc.

Fig. 27.— Cross Section of Epithelial Cokd. Max.

I, Peridental Membrane. W, Epithelial Debris or Cord. EC), Endarteritis Obliterans.

of the peridental membrane, and owing to the position of the
debris at the upper part of the follicle, it would be natural to find
most of it at the peridental membrane.

BONE BUILDING AND ABSORPTION.

Development of the alveolar process is relegated to a series
of cells situated in the fibers of the peridental membrane or
fibrous tissne, and close to the margin of the bone tissue, and

INTERSTITIAL GINGIVITIS.

throughout the Haversian canals. These cells are called the
osteoblasts. They perform the function of building up the bone
tissue. Even after the alveolar process has developed its normal
shape, so unstable is the nervous system which presides over
these cells at this locality, that at the slightest provocation, either

X 560. No. 2 projection ocular. One-twelfth obj. Zeiss.

Fig. 28. — Cross Section Epithelial Cord. Doo.

I, Peridental Membrane. W, Epithelial Debris or Cord. U, Nerve Tissue.

local or constitutional, they will continue their process of con-
struction. Hence, the frequency of hyrjertrophy of the j^rocess,
and in disease the calcification of the peridental membrane.

On the other side of the membrane, next the root surfaces,

TRANSITORY STRUCTURES. 61

may be seen other ceils which build up and destroy the cemen-
tum; these arc called cementoblasts and cementoclasts. These
arc of little importance in this connection with the study of this
disease, although they are frequently present and at work when
inflammation of the membrane occurs.

There is, however, another class of cells found in the peri-
dental membrane of the utmost importance in this connection,
the osteoclasts, located in the fibers, and in close proximity to
the alveolar wall, and around the inner border of the Haversian
canals. The function of these cells is to tear down irregular
bone and tooth structure due to unstable nervous tissue, and from
the slightest irritation.

The gums, mucous membrane, alveolar process and peridental
membrane, owing to their transient nature, are influenced by the
slightest irritation. This influence is the result of both constitu-
tional and local causes. It consists of an irritation in the periph-
eral nerves which sets the osteoblasts and osteoclasts at work
to build up or tear down the alveolar process. This influence
may be only sufficient to stimulate these cells to action without
inflammation. This is noticed in the advance toward old age in
long, lingering debility, in the development of bone, especially
the tearing down and the building up of the inferior maxillary
backward. It may be noted in mild or intense inflammation of
the peridental membrane, due to more acute forms of disease, to
scurvy, mercurial, lead and iodide poisoning, or to local irrita-
tion. So sensitive are these structures that in neurotics and
degenerates the slightest irritation produced in the physiologic
development of the permanent teeth is sufficient to start the
osteoblasts to building up bone structure, thus producing that
pathologic condition called hypertrophy of the alveolar process;
one of the most marked evidences of an unstable nervous
system.

The breaking down of the tissues by the osteoclasts may be
induced by as slight a cause. The alveolar process being so thin
about the teeth, destruction of the entire walls is accomplished
without difficulty, and in a very short time, thus loosening the
teeth, which eventually drop out.

According to Kaufmann 1 the following processes take part in

1 Pathologische Anatomie.

IXTEESTITIAL GINGIVITIS.

the absorption of bone: (a) Lacunar Absorption, (b) Forma-
tion of Perforating Canals, (c) Disappearance after Prior
Absorption of Lime (Halisteresis) (Bony Waste) and Osteo-
malacia.

"By far the commonest form of bone destruction is by lacunar
absorption. This process occurs not only under physiologic
conditions, but is extraordinarily frequent in pathologic states,
e. g., in the various types of atrophy. They form on the
smooth, superficial surfaces of the bone deep grooves (so-called
Howship's lacunas) in which lie smaller or greater polynuclear
cells (osteoclasts, Kolliker) which evidently blend together (Fig.
29). There are no alterations of the bone substance that would

Fig. 29.

a, Bone Trabecular b, Tubercle with Granulation Tissue, e, Broken-down Tissue.
d, Blood Vessel, e, Osteoclasts. /, Fat Cells.

indicate a primary line of absorption (Plummer). The con-
fluence of these lacunae form larger cavities.

" The second form of bone absorption, which is occasionally
met under physiologic conditions, is by means of perforating
canals (so-called Volkmann canals). Under physiologic condi-
tions canals occur in varying numbers in the lamella? (general
lamella?) which contain vessels (perforating vessels). These are
often associated with the Haversian canals and gradually pass

TRANSITORY STRUCTURES. 63

into them, but unlike them, are surrounded with circular lam-
ellae. Under pathologic conditions the conception of these per-
forating canals is somewhat widened. On the one band
Volkmann's canals are spoken of when reference is made to the

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a, Large Spaces Resulting from Absorption of the Trabecule. b, Decalcified Bone,
c and d, Decalcified Bone and Atrophied Trabecule. e, Haversian Canals.

vessels or vascular connective tissue penetrating from one medul-
lary space in the spongy substance, or from one Haversian canal
in the compact substance, to another, in such ;i way that ;i passage
i.s made from one part of the hone to the other; Volkmann's
canals also include irregular ampula-formed dilations or cavities

•64 INTERSTITIAL GINGIVITIS.

(Fig. 30). By confluence of these are produced cavities or irreg-
ularly outlined canals penetrating the bone substance. These, if
they empty into the medullary space, become filled with cells.

" Under much rarer conditions, especially in senile marasmic
osteomalacia and also in that occurring in pregnancy, bone
absorption takes place after a prior abstraction of lime (halister-
esis) and the remaining substance (bone cartilage) is then further
dissolved, passing through a temporary fibroid stage. This
destruction of the decalcified and interfibrillse decomposed bone
is produced as a rule without osteoclasts. The decalcified border
zones of the trabecular appear with simple carmine (coloring) or
by double stains."

CHAPTER IV.

THEORIES OF INTERSTITIAL GINGIVITIS.

The etiology of interstitial gingivitis, according to the views
summarized previously, is divisible into local and constitutional.
While one school leans largely to the local etiology, another
advocates as strongly the constitutional theory. In a general
way. etiology may he divided into exciting and predisposing.
Etiology may also depend upon an element dependent on the
exciting cause, an element dependent on the constitution of the
individual attacked, and finally an element dependent on his
condition when attacked, both as regards his general system
or any one of his organs. The chief constitutional causes to
which the disease has been ascribed are general conditions of the
health, heredity, constitutional disorders, excessive lime salt
secretion, meat-eating, nervous exhaustion, scorbutus and uric
acid states, as well as environment. The local causes assigned
are acute inflammation of the mucous membranes, catarrhal
states, germs or fungi, irregular teeth, lactic acid, pocket dis-
ease, hemorrhagic deposits, seminal calculi and uncleanliness.
That all these factors exercise an influence is undeniable, but
the enormous etiologic role which has been assigned to some of
them is the result of generalization from too few cases. Many
of the assigned causes could lie compressed into fewer etiologic
influences. Thus meat-eating and the uric acid states are too
intimately connected to be regarded as different causes, from a
constitutional standpoint. As has been already pointed out, uric-
acid acts, when it acts at all. like lactic and other acids, as a local
irritant rather than as the constitutional condition (as many -ii|i-
pose) which underlies its production and of which it serves as an
index.

Scorbutus is an expression of a nutritional disorder due very
frequently in the adult to an excess of meat or a monotony of
diet. It is a constitutional disorder, peculiarly apt to have its
local expression in the gums long ere the general constitutional

66 INTEKSTITIAL GINGIVITIS.

symptoms are manifest. The germs and fungi etiologists, on the
other hand, tend to ignore the constitutional state behind the
local culture medium, which must be furnished before growth of
the germ or fungus can occur. In order, therefore, to determine
whether an alleged cause be exciting or predisposing and what
is the influence of the etiologic moment, as the union at one time
of the two constitutional factors already cited is called, analysis
is required of all the varied factors charged with producing the
disease. The influence of heredity is generally left out of con-
sideration unless it be direct, which it rarely is, since heredity,
as has been well remarked, is usually a prophecy rather than a
destiny. It hence constitutes, as a rule, a predisposition.

The chief tissues concerned in the elimination of waste prod-
ucts are the skin, the lungs and air passages, including the
mouth and nose, the kidneys, liver and intestines. Interference
with the eliminatory powers of the kidneys, liver and intestines
is especially apt to throw extra work on the skin, lungs and air
passages. Of this a sour-winey odor of the breath in diabetes is
an excellent illustration. What is true of such a marked form
of suboxidation, resulting in auto-intoxication, is true of less
pronounced forms. The peculiarly foul odor of the breath and
skin in fsecal intoxication indicates that the mucous membranes
of the nose, throat, mouth and gums are doing the work of
elimination which should have been done by the intestines.
The failure of the kidney to perform its share of eliminatory
work is most apt, however, to find expression in the skin, lungs,
nose, mouth and gums.

The influence of the nervous system on the growth and
repair of any tissue is admitted by every physiologist. This
influence is entitled the trophic function of nerves. It is not,
however, exactly settled whether it be exerted through the
nerves themselves or secondarily through their control of the
vaso-motor (blood vessel) system. Many trophic disturbances,
as J. Collins 1 remarks, are probably due to vaso-motor changes,
and it is not possible to separate by any sharply defined line the
vaso-motor from the tropho-neuroses. At the same time, it
should be distinctly remembered that there exist tropho-neuroses
in which there are no appreciable vaso-motor change as in many

1 Nervous Diseases, by Dr. F. X. Dercum.

THEORIES OF INTERSTITIAL GINGIVITIS. f > /

cases of acromegaly and hypertrophies. On the other hand,
there are any amount of vaso-motor disturbance which arc by
no means trophic in character. Trophic disturbance, which may
play a very important part at the onset of interstitial gingivitis,
is neurotic oedema due to nerve irritation. While this is most
frequent on the face, lips, tongue, pharynx, forehead and genital
organs, it also appears on the gums. The oedema reaches its
full development from one-half to two hours. There is a feeling
of stiffness and unyieldingness, but no sensation of inflammatory
swelling. This type of trophic disorder often initiates changes
in the mucous membrane which may readily form the basis of
interstitial gingivitis. This condition may not be only due to
ordinary nervous causes, but may arise from constitutional con-
ditions, gout, etc., and toxic influences.

CHAPTER V.

URIC ACID AND INTERSTITIAL GINGIVITIS.

AVhat John Fitzgerald 1 calls the gingival organs, possess, as
he remarks, in common with some other tissues of the body, the
power of selecting and excreting poisonous substances from the
blood. Some of these cause hyperemia, or even inflammation, in
their passage. Uric acid has been found to play a part in so-
many excretions that it has naturally attracted attention here.
The trend of medical opinion has set strongly in this direction,
but of late this trend is changing.

During the past two decades uric acid has assumed again the
prominence in pathogeny which it once had when called sup-
pressed gout. It is not surprising, therefore, to find that Reeves,
Pierce, Kirk, Rhein and others claim a uric acid etiology for
interstitial gingivitis. In support of this claim are advanced the
results of three experiments which Pierce has had made on
tooth deposits. These deposits were examined chemically by
Ernst Congdon, of the Drexel Institute. 2 The first specimen
contained a number of needle crystals of calcium urate, a few
crystals of free uric acid and crystals of calcium phosphate.
Destructive distillation gave a strong amnionic reaction. The
murexid test for uric acid and its compounds gave faint results,
although its characteristic color was evident in several places.
The second specimen presented the same crystals. The reaction
to the murexid test was strong and resulted in a number of
purplish-red spots. Similar results were obtained from the third
specimen. A. B. Brubaker examined six or eight specimens
in Pierce's presence, with like results to those obtained in the
previous examination. In three an abundance of sodium urate
crystals was present.

The great deficiency in the experiments thus described is the
small number of cases examined and the lack of jDroper control

1 The Clinical Journal, March 1, 1899.

2 International Dental Journal, Vol. XV, pages 1, 217, 501.

ORIC ACID AMI [NTEKSTITIAL GINGIVITIS. 09

experiments. These elements have so frequently led to errors in
dental pathology that I determined upon a series of investigations
in two different laboratories, whose results were reported some
years ago. 1 The Columbus Medical Laboratory was selected for
one series of experiments in special cases. The laboratory of the
Northwestern University Woman's Medical School was selected
for the other series of experiments, to which teeth were sent as
soon as they were obtained. One hundred and fifteen teeth were
sent to the laboratory last named from three institutions in
Chicago which make a specialty of extraction. These teeth had
no history other than the fact that the cases were well-marked
instances of interstitial gingivitis with plenty of calcic deposits,
and that the teeth were loose in the sockets when extracted. ( )f
the one hundred examinations made in the Columbus Medical
Laboratory, fifty were upon specimens of calcic deposits from my
patients and fifty were upon specimens obtained from the institu-
tions just mentioned, and were therefore without history. The
tests employe! 1 were the hydrochloric acid, the dry distillation,
and the murexid, these being the tests recommended by Pierce.
The examinations in the Columbus Medical Laboratory were
made by J. A. Wesener, and those in the laboratory of the
Northwestern University Women's Medical School by J. H.
Salisbury.

Of the one hundred and fifteen examinations made at the
Northwestern University Woman's Medical School by the first
test, in only two case- was found the needle-shaped crystals, and
one in which there was a slight resemblance of uric-acid crystals.
By the dry distillation test, thirteen gave no reaction from
ammonia, and in seven the reaction was slight. The remaining
eighty gave a decided reaction. By the murexid test, four gave
a slight murexid color, hut remainder gave no reaction. Special
examination was made of twelve of these teeth by the addition
of strong hydrochloric acid, warming, decanting the acid, and
washing with water. These gave no reaction by the dry distilla-
tion tests for ammonia. Two gave a slight reaction by the
murexid test. In examination of the teeth of three uric-acid
diathetic women, over forty years of age, uric acid was not

1 Dental Cosmos, April, 189(5, page 310. Journal of the American Medical Asso-
ciation, January 16, 1897.

70 INTERSTITIAL GINGIVITIS.

detectible either by the murexicl test or microscopically. The
examinations made in the Columbus Medical Laboratory were
still more interesting, since among them were specimens from
patients whose history could be obtained. Of the fifty obtained
outside, eight gave positive results from all three tests. The
other forty-two were positive by dry distillation, and negative by
the murexid and microscopical tests. Of the fifty patients,
thirty-eight females and twelve males, thirty-two were over forty
years of age, twelve over thirty years, and six over fifteen years.

Twenty-six have uric acid to a greater or less extent, nine
suffer with indigestion, seven of which are subject to sick head-
ache, thirty-four have rheumatism. Six are English, and four of
these have the true gout ; the other two have rheumatism.

All are positive with the dry distillation test, All are nega-
tive with the murexid test. Forty-nine are negative with the
microscopical test, One shows needle-shaped crystals, but not
uric acid. It is a singular fact that in both laboratories, the
cases in which there was uric acid and gouty histories gave nega-
tive results. By the dry distillation test, out of two hundred
and fifteen cases, all but twelve cases (which have been treated
to remove nitrogenous material) responded. The twelve cases so
treated did not respond, since nitrogenous compounds in and
about teeth (even the saliva) burned to an ash will produce
ammonia. By the murexid test only twelve out of the two
hundred and fifteen gave a jDositive reaction. By the micro-
scopic examination but ten showed crystals. One of the chemists
who made the examination is positive that they were uric acid
crystals. The other is not, since lime-phosphate crystals resemble
uric acid crystals too minutely to be distinguished positively.

For three years Wesener made further examinations as to the
relative value of the three tests employed. According to his
experiments the murexid test is the most valuable, the crystal
test second, and the dry distillation third. The murexid test is
the most reliable in testing tartar for uric acid, since its red color
is easily distinguished from other colors and the test is simple in
application. The test for crystallized uric acid is very unsatis-
factory, since here must be dealt with a complex mass which not
only contains crystals of calcium phosphate (very similar to those
of uric acid) but a great mass of detritus obscuring the crystals

URIC ACID AXD INTERSTITIAL GINGIVITIS. 71

of uric acid. If crystals be present the)' by no means settle the
existence of uric acid. When the faintest quantity possible of
uric acid is mixed with tartar from teetb and subjected to crystal-
lization, the results are always negative. If subjected to the
murexid test, the results are always positive. The dry distilla-
tion test is so inaccurate as to be unworthy consideration.

Since these results were published, seven hundred and thirty-
five cases have been examined. These examinations were con-
ducted by Jerome H. Salisbury, now of Rush Medical College.
The teeth procured from institutions which make a specialty of
extracting contained the dark calcic deposit above the pus line.
By the murexid test, six out of the three hundred gave a distinct
reaction ; eighteen showed crystals under the microscope. The
murexid test was performed as follows: The deposit was selected
as carefully as possible, removed from the tooth, and placed in a
small porcelain crucible. A drop of pure nitric acid was added
and the mixture evaporated on the water bath. When dry, the
evaporation was repeated with another drop of nitric acid, and
the crucible allowed to cool. When cool, the color produced by
the nitric acid was observed, and then a glass rod, wet with
ammonia water, was brought near the deposit, and any color pro-
duced was noted. If no color was observed, the ammonia was
allowed to flow over the residue. A yellow color was produced
in many cases by the nitric acid, which was deepened by the
addition of ammonia. The microscopic examination was made
by scraping off the deposit and evaporating it with a drop of
hydrochloric acid. The residue was moistened with water, and
the insoluble material placed on a slide and covered with a
cover-glass. It was examined with a No. 7 objective. Uric
acid, therefore, occurred in a certain very small proportion of
cases of calcic deposit on the teeth.

Four hundred and thirty-five cases were later examined, mak-
ing in all nine hundred and fifty. Out of these four hundred
and thirty-five cases only four per cent showed uric acid by the
murexid test and eight per cent by the crystal test. Since the
crystal test is not so accurate as the murexid test, it is safe to say
that six per cent was the actual pel- cent of uric acid. A- a
result of the different experiments, in the first two hundred and
fifteen cases five per cent uric acid was found. In the second

72 INTERSTITIAL GINGIVITIS.

three hundred cases, four per cent, and in the third four hundred
and thirty-five cases, six per cent was found. In an examination
of nine hundred and fifty cases by different chemists at different
periods, five to six per cent give positive results as to uric acid by
the chemic and microscopic examination. These results demon-
strate conclusively that interstitial gingivitis is not due solely to
uric acid ; that uric acid when found is merely an expression of
the uric acid diathesis and a coincidence, since it is not always
present in the gums and tartar of patients attacked either by gout
or the uric acid diathesis. In the six per cent of cases there was
nothing to show that uric acid was the cause of interstitial gingi-
vitis, since the deposits were examined after the teeth had been
removed. Any other irritation may have been the exciting-
cause. Uric acid acts, when at all, solely as a local irritant.

CHAPTER VI.

INORGANIC SALTS AND INTERSTITIAL GINGIVITIS.

The foods which enable the body to repair its waste, to build
up new tissue and to supply the energy, arc divisible into four
classes: the inorganic substances, the fats or hydrocarbons,
and the starches and sugars, or carbohydrates, and the proteid
compounds. These divisions are, however, relative, since the
proteids may contain both hydrocarbons and carbohydrates.
The inorganic substances, such as water, phosphates, chlorides,
carbonates, sulphates, etc., enter the body, as a rule, under their
own form, either alone or in combination with other classes.
They are not oxidized or split up within the system to enter into
the chemical formations of other compounds, but are united
mechanically with the proteid group. These bodies act, as a rule,
in a purely mechanical manner. After having served their pur-
pose, they pass out of the system with the excretions, compara-
tively unchanged in their composition. They are the only
mem her of the group of foods which are of a special interest in
the present research. The inorganic salts have, however, not
received the attention from physiologic chemists that their
importance demands. They are, as a rule, found in greater or
lesser quantity in all foods that are taken into the body. They
do not serve as a source of energy, but as the other foods are
needed for the development of the tissues, so the inorganic salts
are needed for the building of bone tissue and the repair of

waste. This is accomplished by the soluble salts in the 1>I I.

Human blood has the following composition :

ANALYSIS OF HUMAN BLOOD (C. SCHMIDT). HOWELL'S
PHYSIOLOGY.

Max. Woman.

25 Years. 30 Years.

Water 788. 71 824. 55

Solids 211.29 .... 175.45

Proteids and Extractives 191.78 .... 157.93

Fibrin 3.93 1.91

Htematin (and iron) 7. 70 .... 6. 99

Salts ' 7.88 .... 8.62

74 INTERSTITIAL GINGIVITIS.

INORGANIC SALTS OF HUMAN BLOOD, 1,000 PARTS
(C. SCHMIDT).

CI ..

,OOD

CORPU

SCLES

1.75

3.091

0.470

0.061

1.355

CI . ..

Blood

\SMA

3.536
314

NA 20

NA 20 .

SOg

3.410

SO,

0.129

CaO

M t „, .

■P'205 • •

CaO .

M qn . . .

0.145

These acids and bases exist, of course, in the plasma and the
corpuscles as salts. It is not possible to determine exactly how
they are combined as salts, but Schmidt suggests the following
combination :

PROBABLE SALTS IN THE CORPUSCLE.

Potassium Sulphate 0. 132

Potassium Chloride 3. 679

Potassium Phosphate 2. 343

Sodium Phosphate 0. 633

Sodium Carbonate 0. 341

Calcium Phosphate 0. 094

Magnesium Phosphate 0. 060

PROBABLE SALTS IN THE PLASMA.

Potassium Sulphate 0:281

Potassium Chloride 0.359

Sodium Chloride 5. 546

Sodium Phosphate 0. 271

Sodium Carbonate 1. 532

Calcium Phosphate 0.298

Magnesium Phosphate 0.218

It will be seen that the corpuscle contains an excess of
potassium salts, and the plasma contains an excess of sodium
salts. All parts of the blood contain salts, however.

Throughout the entire body, there is a rich supply of blood
vessels penetrating every tissue. The plasma of the blood pass-
ing by exosmosis through the walls of the capillaries is thus
brought in immediate contact with the tissues to which it brings
nourishment and oxygen of the blood, and from which it
removes the waste products of metabolism. Other usable prod-
ucts or lymph are collected in small capillary spaces, which in
turn open into definite lymphatic vessels. These vessels unite

URIC ACID AND [NTERSTITIAL GINGIVITIS. VO

into larger and larger one*, which eventually pour this usable
waste product into the great thoracic or left lymphatic ducts, and
a second smaller right lymphatic duet. These in turn empty
into blood vessels, each upon its own side. The lymph contains
essentially the same constituents as the blood plasma, and the
salts are found in the same proportion as in it. They are then
eliminated through the sweat glands, tonsils, mucous glands,
kidneys, large intestines and salivary glands.

The composition of the deposits in the various parts of the
body vary according to the locality and the character of the
excreta eliminated in connection with them.

The chemical composition of the human bile, according to
Jacobson, 1 is as follows :

Water 977 . 40

Sodium Glycocholate 9 . 94

Cholesterin 0.54

Free fat . 10

Sodium palmitate and sterrate 1 . 26

Lecitine a . 04

Other organic matter 2 . 2t>

Sodium chloride 5 . 45

Potassium chloride 0.28

Sodium phosphate 1 . 33

Lime phosphate 0.37

Sodium carbonate . 93

Of this analysis the solid ingredients constitute 22.5 parts per
thousand, of which two-thirds are organic and one-third inor-
ganic. The inorganic salts of the bile are in most cases returned
to the blood, where they are redistributed to the tissues. Occa-
sionally, however, gall stones occur, which are composed of
(analysis H. I). Geddings 2 ):

Moisture 3 . 32

Biliary matter 32 . 182

Cholesterin 54 . 952

Matter soluble in ether 7.77

Iron traces

Phosphoric acid traces

Lime traces

Magnesium traces

1 American System of Dentistry.

2 Transactions 8outh Carolina Medical Association, 1SS0.

76 INTERSTITIAL GINGIVITIS.

Secretions of the pancreatic juice (dog) by C. Schmidt are as
follows :

Water 900 . 76

Solids 99 . 24

Organic substances 90 . 44

Ash 8.80

Sodium carbonate . 58

Sodium chloride 7 . 35

Calcium magnesium and sodium phosphate . 53

The composition of the normal human pancreatic juice has
not been determined completely owing to the difficulty of obtain-
ing the secretion. According to Zawadsky the composition of
the secretion of a young woman was as follows :

Water in 1.000 parts 864.05

Organic substance in 1,000 parts 132 . 51

Proteids in 1, 000 parts 92 . 05

Salts in 1, 000 parts 3 . 44

INORGANIC SALTS IN THE SWEAT.

" Of the inorganic salts, NaCl is by far the most abundant ;
it occurs in quantities varying from 2 to 3.5 parts per thousand.
The elements of the sweat which are of importance from an
excretory standpoint are water, inorganic salts and urea or related
nitrogenous compounds."

Inorganic salts from the faeces are made up of the salts of
sodium, potassium, calcium, magnesium and iron. According to
Enderlin 1 the following represent the composition of the material
matter in the faaces :

SALTS SOLUBLE IN WATER.

Sodium chloride and sulphate 1 . 37

Sodium phosphate 2 . 63

SALTS INSOLUBLE IN WATER.

Earth phosphate 80 . 37

Ferric phosphate 2 . 09

Calcium sulphate 4 . 53

Silicic acid 7 . 94

Like other constituents of the lymph, the salts vary consider-
ably in proportion, according as the fluid is more or less rich in

1 Gamgee, Physiological Chemistry of the Animal Body.

URIC ACID AND INTERSTITIAL GINGIVITIS. 77

water. The salts are much more abundant than the organic
solids.

Inorganic salts in the urine consist, according to Howell, 1
chiefly of chlorides, phosphates and sulphates of the alkalies and
the alkaline earths. As a rule they arise partly from the salts
ingested with the food, which salts are eliminated from the blood
by the kidney in the water secretion, and in part they are formed
in the destructive metabolism which takes place in the body,
particularly that involving the proteids. Sodium chloride occurs
in the largest quantities (about 15 grams per day), of which the
greater part is derived directly from the salt taken in the food.
The phosphates occur in combination with Ca and Mg, but chiefly
as acid phosphates, of Na or K. The acid reaction of the urine
is caused by these latter. The phosphates are produced in part
from destruction of phosphorus-containing tissues in the body,
but chiefly proceed from phosphates in the food. Following are
the average quantities in grams of the chief substances normally
excreted in the urine in six hours r

Water 1440 — 1500

Solids 57 — 68

Organic :

Urea 28 — 68

Uric acid 7

Hippurie acid 3 — 2

Kreatiniu 1.7 — 2.1

Inorganic :

Sodium chloride 15 — 20

Phosphoric acid 2.5 — 3

Sulphuric acid 2 — 2.5

Sodium 5 — 7

Magnesium .04

Potassium 3 — 4

Calcium .03

Urinary calculi (classified according to their principal ingre-
dients), are divided into :

1. Uric stone, composed of uric acid and acid urates.

2. Oxalic stone, composed of lime oxalate.

3. Phosphoric stone, which are composed of magnesium phos-
phate and carbonate with urate of ammonia.

1 American Text-Book of Physiology.

2 Landolt, Physiology.

78 INTERSTITIAL GINGIVITIS.

Each one of these compounds is nearly in a pure state. A
stone may be composed entirely of one salt or it may be composed
of two, three or four, each compound forming separate consecu-
tive layers through the stone. One examination made by How-
ship Dickinson 1 showed eighty-nine per cent lime carbonate and
the rest lime oxalate and phosphate of lime.

The deposits upon the teeth are derived partly from the salts
ingested with foods, which salts are eliminated from the blood in
water secretion, and in part they are found in the waste of tissue
which takes place in the body.

The saliva, according to Schmidt, is made up of the following :

Water 991 . 45

Organic material 2 . 89

Inorganic :

Calcic chloride 4.50

Sodium chloride ....

Calcic phosphate 1.16

Magnesium ....

1,000.00

This material floating in the saliva, together with the epithe-
lial scales and other extraneous matters, contribute to form what
is known as tartar. This material collects upon the teeth, and
according to examinations by Stevenson consists of:

Soft tartar Hard tartar

on molars. on lower incisors.

Water and organic matter 21 . 48 .... 17 . 51

Magnesium phosphate 1.31 .... 1.31

Calcium phosphate with a little car-
bonate and trace of fluorine .... 77 . 21 .... 81 . 18

100.00 .... 100.00

Another analysis made by Scheheoetskey resulted thus :

Water and organic matter 22. 07

Magnesium phosphate 1 07

Calcium phosphate 67.18

Calcium carbonate 8.13

Calcium fluoride 1.55

100.00
1 Renal and Urinary Affections.

URIC ACID AND INTERSTITIAL GINGIVITIS. 79

Malenfant found that salivary calculi (located in Wharton's

duct) was composed of:

Lime phosphate 27

Magnesium phosphate 1

Basic lime phosphate 60

Alcohol and muriatic acid 4

Ptyalin 2

Loss 6

100
The following are results of analysis of salivary calculi by
various observers :

Weight.

100 Parts.

Bivra.

Lecanu.

Besson.

Golding

2 3

Bird.

Calcium carbonate. . .

81.2

79.4

80 . 7

13.9

Calcium phosphate . . .

4.1

5.0

4.2

38,2

Magnesium phosphate

5.1

Soluble solids

Organic matter

6.2
7.1

4.8
8.5

5.1)
8.3 j

38.1

Water and loss

1.3

2.3 1.7

6.3

Deposits in the tissues in gout are made up of soda and lime
urates. In order to compare the calcic deposits in other parts of
the body with the serumal deposits upon the teeth affected with
interstitial gingivitis, thousands of teeth were obtained from three
dental offices which make a practice of extracting teeth. From
these one thousand were selected at two different times, making-
two thousand teeth containing deposits direct from the tissues.
These were submitted to a chemical analysis by J. H. Salis-
bury, at Rush Medical College, who reports as follows :

" The method which I employed in analysis of calcic deposits
was as follows : The material was so selected as to be free as
possible from salivary tartar and a weighed portion was dried at
100° C. This was then carefully incinerated and again weighed,
and the difference calculated as organic matter. The residue
after incineration was divided into two portions, A and B.

"A was used for the estimation of phosphates as follows :
The ash was dissolved in nitric acid and the solution precipitated
with ammonium molybdate. The precipitate was washed, dis-
solved in ammonia precipitated by magnesia mixture and the

$0 INTERSTITIAL GINGIVITIS.

precipitate of ammonia magnesium phosphate, washed, dried,
ignited and weighed.

" In B, calcium and magnesium were estimated as follows :
The ash was dissolved in hydrochloric acid and the acid just
neutralized with ammonia water and sodium acetate added. It
was then made slightly acid with a drop of hydrochloric acid
and precipitated with ammonium oxalate. The precipitate of
calcium oxalate was filtered off, washed, converted into calcium
oxide and weighed. The nitrate was made alkaline, sodium
phosphate added, and the precipitate of magnesium-ammonium
phosphate collected, washed, dried, ignited and weighed. In
case the phosphoric acid determined in A did not saturate the
calcium and magnesium obtained in B, the excess of base was
calculated as carbonate.

" The following is the composition of the serumal tartar
according to analysis of April 18, 1898 :

Water and organic matter 32 . 24

Magnesium phosphate 98

Calcium phosphate 63 . 08

Calcium carbonate 3.70

100.00

"Analysis of the serumal tartar, October 24, 1898, shows it to
have the following composition :

Water 4.48

Organic matter 27 . 00

Calcium phosphate 72 . 73

Magnesium phosphate 4. 91

99.12

While nearly every kind of food taken into the stomach con-
tains inorganic salts, every excretory organ of the body throws
out a certain amount of these salts. Some of these organs
excrete the salts in a pure state, while in others the salts are
combined with acids or fluids peculiar to that organ. These salts
differ in composition and quantity on different days, at different
hours of the same day ; differ at different ages of the same person
and differ in persons of like age, on the same diet. No matter
how careful the chemist may be in analysis, no two results will
be exactly alike. For this reason, in tartar and calcic deposit

URIC ACID AM) INTERSTITIAL GINGIVITIS. 81

upon the roots of teeth, two different analyses of the same deposits
are cited. It is evident that while slight differences occur in the
table, these are due chiefly to the character of the secretions.
The kidneys and salivary glands clearly excrete most of the waste
inorganic salts.

Since each excretory organ has its part in elimination of
waste inorganic salts, it is clear that if one organ becomes tired
or diseased, other organs have an extra amount of material to
excrete. In any event, the blood becomes surcharged with waste
inorganic salts. There is a class of patients with deformed jaws
and irregular teeth, tonsil hypertrophy, mucous membrane,
nasal bone and post-nasal space disorder, adenoids, arrest of the
facial bones. They are neurotics and degenerates. This class
comprehends those whose nervous system is unstable and whose
physical development is a departure from the race type. This
unstable or tired condition may affect but one excretory organ.
In most cases it affects all organs as well as the entire body. In
these patients, especially in youth, does hypertrophy of the alve-
olar process take place and large deposits are observed upon the
teeth. In this class may be placed rachitic children.

Inorganic salts taken in food are generally utilized until the
osseous system has attained its growth. This usually occurs at
about the twenty-sixth year, but full growth may not be attained
until the thirty-sixth year. When this period has been reached,
although the body still has the same supply of inorganic salts,
the system can assimilate only what it needs. The remainder
becomes waste. Under such conditions the blood is overcharged
with these salts.

A condition of the system, which has received too little atten-
tion, occurs in a class of children ranging from six to eight
years, who excrete larger quantities of inorganic salts through
the kidneys and salivary glands. In such cases the teeth
become coated with tartar. The gums become inflamed from
irritation. Interstitial gingivitis is developed in youth. These
children may be rachitic, or border upon the disease. They are
neurotic, degenerate, suffer from rachitis, rapid decay of the teeth
and irregularities. They occur in American and European
schools of idiocy and for dependent and defective children.
From seventy-five to ninety per cent of these children have

82 INTERSTITIAL GINGIVITIS.

interstitial gingivitis, ranging from simple inflammation of tli e
gums to absorption of the gums and alveolar process with pus
exudate. Miller noticed in an examination of twenty-six cases
of rachitic children under twelve years of age that seven mani-
fested pronounced symptoms of interstitial gingivitis. This was
no doubt due to accumulation of calcic salts upon the teeth,
producing irritation and absorption of the alveolar process and
contraction of the gums.

In cases where large collections of tartar are deposited upon
the teeth of children there is also an excess of excreta through
the kidneys. Examination of urine in such cases will reveal
always from four to eight times more deposit than the normal
for the age of the patient. Defective nutrition is the result, the
bones are small, and the jaws and teeth are irregular. The teeth
decay early in life and it is with difficulty that the decay can be
arrested. What is true of children is also true of people at
advanced age.

'After the skeleton had attained its growth (even in those
cases where no deposits were before observed) the blood became
overcharged with lime salts and the teeth became a nidus for the
deposit from the salivary glands. It is, therefore, clear why
deposits and inflammation of the gums are so common after the
twenty-sixth year, and more common later in life. Defective
children and people who have obtained their growth are more
susceptible to trophic disorders of nutrition and the tissues take
on disease more readily than healthy individuals earlier in life.
When inflammation takes place in connective tissue in all parts
of the body (especially if the blood be surcharged with inorganic
salts) deposits take place in that tissue through the capillary
system. On the other hand, when inflammation of the connective
tissue takes place, if inorganic salts be scarce in the blood,
deposits do not take place. As is elsewhere shown, 1 calcic
deposits on the roots of teeth are a result of inflammation and
pus infection and not the cause.

1 International Dental Journal, April, 1S96.

CHAPTER VII.

HEREDITY AND ENVIRONMENT.

The influence of heredity in interstitial gingivitis, as in other
morbid conditions, is still a mooted question. Morbid heredity,
as I have elsewhere shown, 1 is practically divisible into direct and
indirect. In the first type the morbid condition is directly inher-
ited ; in the second, a deficiency is due to the morbid condition
which may or may not express itself in a tendency to the morbid
condition of which it is the offshoot, Heredity further should he
separated from congenital states which result from the operation
of germs or toxins during a particular pregnancy wherein these
pass through the placenta to the foetus. A child may he born of
a tuberculous mother with a tendency to tuberculosis, but the
tubercle bacili may also directly infect it through the placenta so
that it is born with tuberculosis. The first is the inheritance of
the weakened organism of the mother. The second is a condition
of intra-uterine infection.

The reported cases of direct heredity of the pyorrhoeic stage
of interstitial gingivitis may afford instances of one or the other of
these- categories. As has elsewhere been shown, transitory organs
are peculiarly apt to lie weakened by heredity both in their
structure and in their resistance to morbific germs and agencies.
These weaknesses . are especially apt to he shown during the
period of systemic stress connected with the first and second
dentition. Such weaknesses may lie the outcome of general
nerve exhaustion on the part of the parents (the mother espe-
cially), and constitutes transformed heredity, which is far more
frequent than direct. This transformed heredity may he more
intense than the constitutional deficiency of the immediate
ancestry. .On the other hand, the conservative influence of
several generations may so offset the evil results of the defect- in
the parents that the inheritance of defect is slight, if at all
existent.

Degeneracy; Its Si<_rns. Causes and Effects

84 IXTEKSTITIAL GINGIVITIS.

This last tyr^e of heredity is called atavism (or "throw-back,"'
by the breeders). It is more likely to work for good than evil,
albeit the evil effects are more generally looked for. Because of
this atavism a serious nervous defect in a parent might express
itself only in an increased tendency to disease on the part of
transitory structures. The periods of stress are times in the life
of man when certain great life functions are developing or under-
going retrogression. These periods of development or evolution
are marked by the tw r o dentitions and the development of the
sexual organs, which might more aptly be called the third den-
tition, since ere its close the wisdom tooth appears, if at all. The
periods of retrogression are when the great sexual functions are
undergoing involution or when the whole body is undergoing
senile change. These periods often constitute an etiologic
moment for the production of disease even when potent heredi-
tary defect is absent, albeit at these periods such defect is apt
to appear.

Another possibility to be considered in this connection as
complicating the diagnosis of heredity in disease is environ-
ment, understanding by this term all the external conditions that
can favor the development of a disorder. Family habits and
surroundings are apt to be alike for every member. If anything
in the environment especially favors the breaking out of a disease
in one member, the cause is equally apt to be effective with
another, provided the individual idiosyncrasy is similar. This
may give rise to a suspicion of heredity, since conditions of life,
family habits and intimate household surroundings favor the
occurrence of a disorder in several members or generations of the
same family. Habits are often transmitted by imitation from
parents to offspring. These may be direct exciting or predis-
posing causes of an affection, especially if it be more or less
favored by their existence.

That constitutional 'conditions of hereditary origin favor the
occurrence of interstitial gingivitis is undeniable, but this does
not prove that gingivitis itself is hereditary. They favor its
occurrence as they favor other morbid conditions, by lessening
resistance, or by preparing the way. The gingivitis is only one
of the many accidents that are thus facilitated. So far as sali-
vary concretions are to be regarded as an exciting cause, heredity

HEREDITY AND ENVIRONMENT. 85-

may be disregarded, since these (though varying widely in dif-
ferent individuals in the amount of the deposit, and consequently

the irritation produced) are dependent upon more remote con-
stitutional or loeal conditions without direct connection with the
heredity.

The varieties (charged to lithaemia or arthritic conditions
notoriously hereditary) are of accidental origin rather than essen-
tially connected with constitutional conditions that happen to
furnish the irritant.

Local uric acid poisoning 1 is. as I have elsewhere shown,
occasionally associated with gingivitis. The coexistence illus-
trates the lowered vitality of the system, rather than the
etiology.

The same is true of all the other neurotic, rachitic and degen-
erative conditions, hereditary or otherwise, that are met with,
associate I with gingival inflammation. They all favor the
occurrence of the disease by causing a weakened power of resist-
ance predisposing to the attack of any irritation. The mouth,
resistant as it ordinarily is, is at all times open to irritation. When
resistance is impaired it gives way at its most vulnerable point,.
and the gingival margin is one. Interstitial gingivitis is favored
or hindered, like other disorders of its kind, by constitutional
conditions which may or may not be inherited, and which bear
toward it the relations only of predisposing and accessory
causes.

1 Dental Cosmos, 1890,

CHAPTER VIII.

DEGENERACY AND DEGENERATE TISSUES.

One of the most important factors of predisposition is that of
degeneracy, either local or general. Three possibilities of life
await, as has been elsewhere pointed out, 1 each living being :
either it remains primitive and unchanged, or it progresses
toward a higher type, or it backslides and retrogresses. The
factors underlying the stable state force the animal to remain as
it is ; these underlying the progressive tendency make it more
elaborate, while the factors of degeneration tend to simplify its
structure. Degeneracy is, therefore, a gradual change of
structure by which the organism becomes adapted to less varied
and less complex conditions of life. It is a reverse of develop-
ment which proceeds from the indefinite and homogeneous to the
definite and heterogeneous with a loss of explosive force due to
the acquirement of inhibitions or checks. In proportion to the
depth of degeneracy does it affect the earlier simpler, or later
complicated, acquisitions. The opposite process of progression is
a gradual change of structures by which the organism becomes
adapted to more varied and more complex conditions of life. In
progression there is a new expression of form corresponding to
new perfection of work in the animal machine. In degeneracy
there is suppression of form corresponding to the cessation of
work. Elaboration of some one organ may be the necessary
accompaniment of degeneracy in all the others. On the other
hand, ' degeneracy in one organ may be the necessary accompani-
ment to the elaboration in all the other organs. During the period
of stress defects due to degeneracy are apt to appear and affect the
line of least resistance, determined by the depth of degeneracy,
as well as the variability of the structures concerned. As the
teeth and jaws are among the most variable structures in the
body, they are peculiarly apt to be affected by either general
degeneracy, which affects the body as a whole, and has local

1 Talbot : Degeneracy ; Its Causes, Signs, and Results.

DEGENERACY AND DEGENERATE TISSUES. 87

expressions or local degeneracy by which the body benefits.
The factors producing degeneracy act by causing nervous exhaus-
tion in the first generation. This implies a practical degenera-
tion in function, since tone is lost.

Every nerve cell has two functions; one connected with sensa-
tion or motion, and the other with growth. If the cell lie tired
by excessive work along the line of sensation or motion, the func-
tion as regards growth later becomes impaired. The cell then
not only ceases to continue in strength, hut becomes self-
poisoned. Each of the organs (heart, liver, kidneys, etc.) has
its own system of nerves (the sympathetic ganglia) which, while
under control by the spinal cord and brain, act independently.
If these nerve centers become tired, the organ fails to perform its
functions, the general system becomes both poisoned and ill-fed,
and nervous exhaustion results. In most cases, however, the
brain and spinal cord are first exhausted. The nerves of the
organs are thus allowed too free play, and exhaust themselves
later. This systemic exhaustion has local expression in the
testicle in the male, in the womb and ovaries in the female.
Through this the body is imperfectly supplied with natural
tonics (antitoxins) formed by these structures, and the general
nervous exhaustion becomes still more complete. All the organs
of the body are weakened in their function. Practically the
neurasthenic in regard to his organs has taken on a degenerative
function, albeit not degenerating in structure, since the rest-
lessness of the organs is a return to the undue expenditure of
force which occurs in the lower animals in proportion as it is
unchecked by a central nervous system. Through the influence
of various exhaustion agencies the spinal cord and the brain lose
the gains of evolution and the neurasthenic is no longer adjusted
to environment. Since the reproductive organs suffer partic-
ularly, children, born after the acquirement of nervous exhaus-
tion, are more or less checked in development as the influence of
atavism is healthy or not — have degenerations in the structure
of their organs which in the parent were represented by neuras-
thenic disorder in function. As the ovaries of the neurasthenic
woman generally exhibit prominently the effects of the nervous
exhaustion, the offspring of these do not retain enough vigor to
jiass through the normal process of development.

OO INTERSTITIAL GINGIVITIS.

The action of degeneracy, considered as a local factor of con-
stitutional origin, may be exerted to preserve embryonic con-
ditions in adult life. Such preservation may result in the
breakdown of tissues which would otherwise withstand germs or
other causes of disease external to the tissues. Given this con-
dition of local degeneracy, a local predisposing factor is added
to both the exciting causes and the constitutional predisposing
factors. So long as the teeth and transitory structures remain in
the comparatively stable condition of primitive races, this factor
is to a great extent in abeyance. When, however, the jaw begins
to evolve, the degenerate types find this factor adding dangers to
their evolution. In the degenerate the struggle for existence
between the organs is not properly balanced, whence the dangers
from these local states of degeneracy that in the higher types
are expressions of advance undergone without danger. This is
excellently illustrated in the embryology of the mucous mem-
brane. This in degenerate children often fails so to develop
that the bactericidal function of mucus does not appear. This
hereditary feebleness of the mucous membrane is peculiarly apt
to occur in the nose, throat and gums, but other mucous mem-
branes are not exempt.

CHAPTER IX.

NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN.

Miller, as elsewhere stated, found a little over thirty-three
and one-third per cent on examination of twenty-six rachitic
children under twelve years who manifested interstitial gingivitis.
Considering that most of these manifested symptoms of inherited
congenital or acquired constitutional defect, such a small propor-
tion is rather remarkable. The fact suggests one of two explana-
tions — either the children in the institute visited by Doctor
Miller took better care of their teeth and gums than is usual
with this class, or the cases in which pus existed only were
classed as pyorrhoea. I have examined the mouths of deaf-
mutes, blind, idiotic, feeble-minded and rachitic children in the
institutions in America and Europe. Interstitial _ gingivitis was
found in all its stages, from simple inflammation of the gums to
loosening of the teeth, in from twenty-five to seventy-five per
cent. In these cases not only are there constitutional factors,
but also uncleanliness of the mouth and gum tissues. The
degenerate children encountered in office practice usually have
jaw deformities and teeth irregularities. Patterson has had
under observation thirty-eight cases of well-marked pyorrhoea,
thirty-three of which coexisted with nasal catarrh. These eases
were, no doubt, those of degenerate patients. The nasal catarrh
was a coincidence dependent on the general deficiency of the
mucous membrane.

Luxury and modern degeneracy are generally charged with
the production of diseases later found to have attacked man
in prehistoric periods. This has been the case with interstitial
gingivitis.

R. R. Andrews expresses the following opinion as to modes
of life: "I have been led to believe from my own experience
that this trouble exists largely in the mouths of people accus-
tomed to luxury — good livers, people about middle age who.
over-eat and under-work."

90 INTERSTITIAL GINGIVITIS.

No method of living can be regarded as a cause of this
disease, except so far as it affects the general system, thus pro-
ducing trophic changes. There is probably a slight difference
in liability to interstitial gingivitis between people of sedentary
habits and active outdoor workers, as well as between animals
domesticated or in captivity and those which run at large.

It is, however, obvious, from the data of the chapter upon
tl History," that all races and stations, regardless of time, climate,
or mode of life, have suffered with the disease. Examinations of
animals in the American and European zoological gardens show
that it is not confined to any class of animals. Dogs and cats,
whether housed or running at large, suffer with it.

The question how far this region is affected by toxic agents
introduced into the system is an open one ; still it seems probable
that they exert some influence. In chronic phosphorus poison-
ing the jaw is particularly and seriously involved. This has
been attributed chiefly to the entrance of phosphorus into the
•deeper tissues through carious teeth or through solutions of con-
tinuity of tissue due to tartar. In the case of other poisons this
local factor is not so evident. Mercury has among its first
effects a soreness of the teeth with loosening of them in their
sockets. Here it appears that the alveolus was one of the first
special points of attack independent of any traumatism or
abrasion of the soft tissues. In a similar way the toxins of
scurvy directly attack the alveolus. Its fleshy covering is later
involved in the progress of the disease. This sometimes extends
to complete loosening and falling out of the teeth. Here an
irritation of a toxin from within the organism has a point of
election, a structure that from its constitution or other reason is
particularly vulnerable to attack. Another constitutional dis-
order in which the alveolus is early affected is diabetes. The
exact pathology of this is uncertain, but in many cases at least
it is largely dependent on disordered action of the central nerve
system. Renal disease is another common condition which tests
the vulnerability of the alveoli. An ideally normal kidney is
j^robably rare, but only when its abnormalities pass beyond a
certain point can it be called diseased. In the less advanced
conditions that have passed the line of morbidity, alveolar impli-
cation is often very marked. This may be one cause of the

NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 91

unusual frequency in the insane, who are especially liable (as
Bondurant ' and others have shown) to suffer from renal disease.
They are very Liable likewise to auto-intoxications and trophic
disorders as 2 well, since the balance of the nervous system has
been disordered. Some (the paretic and organic dements)
exhibit especial tendencies to trophoneurotic disturbances affect-
ing the teeth. In states of depression and stupor, circulatory
disturbances predispose to these.

The constitutional results of acute and chronic infections are
apt to produce auto-intoxicatioD in addition to the action of the
toxins of their germs. The eruptive fevers, especially scarlatina
or measles, have been long known to be followed by wasting or
necrosis of the alveoli." Here the condition is notably symmet-
rical and unaccompanied by exfoliation or necrosis of the osseous
system elsewhere. Tuberculosis does not spare the alveolar pro-
cess. The well-developed disorder known as Riggs's disease has
been charged by Robin and Magitot to the direct influence of the
arthritic (gouty and rheumatic) process, and declared a special
form of arthritic manifestation.

The alveolus is clearly vulnerable to the toxins of many
infectious diseases. It is also quickly affected by some of the
autotoxic influences of disordered metabolism. Its vital resist-
ance to these agencies is less than that of other tissues. It is the
earliest sacrifice when these toxins or all toxins disturb the har-
mony of the organism.

Another cause for implication of these parts than the action
of toxins exists. Whenever tissue waste, whether local or gen-
eral, exceeds repair there is trophic change. This latter depends
directly upon disordered local or general nervous functions.
Trophic alterations from the first cause appear in growth disorders
of the nails and loss of hair (alopecia) after fevers — the most
familial' obvious examples of this pathologic process. Of the
other type are localized neurotic atrophies where the direct inter-
vention of toxins can be excluded. The alveolus is liable to the
first form of trophic deterioration. The influence of acute dis-
eases upon the alveolus is probably thus exerted in many casts

1 American Journal of Insanity, 1892.
2 Kiernan, Journal of Nervous and Mental Diseases, 1878.

J Salter : Transactions of Pathological Society, London, 1859-60, Vol. XI, page 309.
Lucas, Lancet, 1887, page 692.

92 INTERSTITIAL GINGIVITIS.

rather than by direct infection. Where no cause has been ascer-
tained, examination directed to this factor would probably reveal
it. The general failure of the trophic centers after the prime of
life (in senile states), which is attended with loss of teeth and
wasting of the alveoli, is perhaps the most prominent instance of
this type of trophic failure affecting the part. Even simple
anaemia may thus rise to alveolar wasting.

The second form of trophic failure in the alveolus is less
prominent since it generally coexists with overshadowing disturb-
ance elsewhere which masks it to a certain extent. C. Cruveilier 1
noticed its occurrence associated with paraplegia and invokes a
nervous influence in its causation. In facial hemiatrophy local
wasting of the alveolus has appeared before the disorder had
involved generally the jaws. This may sometimes be due to a
local cause, but its occurrence and association with other neuro-
trophic symptoms is suggestive.

The causes which, acting locally, produce direct interstitial
gingivitis, are the toxic effects of mercury, lead, brass, uric
and other acids, potass, iodide, and other agencies acting in a
similar manner, and scurvy. It is not the intention to enter into
an elaborate discussion of the toxic action of these drugs, but in
a general way to show the similarity in action and results upon
the tissues. Scurvy, a disturbance of metabolism, produces the
same train of symptoms as the metals.

It is a widespread opinion among dentists that in toxic cases
the gums are the first tissues involved. The fact is, however,
that when the salts of mercury are taken into the system, as
noted elsewhere, they act directly upon the central nervous
system; later occur nausea and vomiting, tremor in the arms and
hands. Besides local nerve inflammation (neurites), mercurial
and brass poisoning produces paralysis agitans, and lead poison-
ing, drop wrist, etc.

Excessive secretions of the glands of the body, especially the
salivary glands, later occur with rise in temperature, gingivitis
with periosteal and j^eridental membrane swelling, thickening of
the gums and loss of the teeth. The central nerve system dis-
turbance affects all other structures. Inflammation of the
mucous membrane of the mouth, as well as of the gums, and of

1 Bak. Soe. de Chir. Paris, 1S70, pages 30 and 31.

NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 93

the alimentary canal, frequently occurs with sloughing of tissue.
The kidneys become involved, and are unable to carry off the
effete matter.

The cachexia, which resembles that of scurvy, is characterized
by great debility, anaemia, emaciation, alopecia, atrophy and
coarseness of the nails, with pain in the muscles and joints.

Mercury is eliminated by all excretory organs for which it
has a great affinity. The soluble salts pass out by the bowels.
So long as the excretory organs of the body eliminate mercury,
the tissues are not effected. Small doses are eliminated, but con-
tinuation of dosage soon involves the nervous system, and after-
wards the tissues of the body, especially the jaw r s. The first
effect of mercury upon dogs is to produce vivacity and animation.
This lasts for two or three days, when the limbs begin to trem-
ble. The kidneys and bowels act at first freely. At the end of
seven or eight days paralysis agitans occurs. There is constant
trembling, whether when awake or asleep; loss of appetite, with
slight rise of temperature. At the end of two w r eeks, the gums
become inflamed at the margins. If the drug be continued,
death occurs in about three weeks. The loss of flesh is remark-
able. Miners working in mercury mines, and looking-glass
makers, are all affected to a greater or less extent. The nervous
system is always involved. The kidneys become diseased. The
hair drops out. The miners think it a happy issue from their
trouble when they have lost all their teeth, or even the molars.
They are henceforth exempt from suffering so far as the teeth
are concerned. Many are toothless at thirty-five.

Mercury taken by the mouth is found in the urine in two
hours, and in the saliva in four hours. It appears in the urine
fourteen hours after it has been applied to the skin. 1 Although
it is believed to have passed entirely out of the system, it has
been found in the brain, liver, kidneys and muscles. It is
claimed that, like lead, it forms combinations with albuminoids
in the tissues, for a time remaining inert, to be subsequently
oxidized and returned to the circulation as an active poison.
While a single dose of mercury may be rapidly eliminated from
the system, repeated small doses distributed over a long period
are not so eliminated on account of the thickness and occlusion

Twentieth Century Practice of Medicine, Vol. Ill, page 935.

94 INTERSTITIAL GINGIVITIS.

of the walls of the capillaries, producing endarteritis obliterans,
hence more or less of it is deposited in the tissue.

Lead enters the system through the alimentary canal, skin
and respiratory tract. A longer time is required to produce
plumbism (lead poisoning) than mercurial poisoning. Lead is
stored up in the system in minutest quantities for an indefinite
length of time. Its effects are not manifest until the central and
peripheral nervous systems have become involved, as evinced
by the effect of plumbism upon the wrists. Occasionally, the
chief seat of deposit is the liver or muscles. It is chiefly elim-
inated through the kidneys, and very slightly through the liver
and salivary glands. Not until a considerable length of time
has elapsed is lead traceable upon the gums. This usually
occurs about the lower incisors and cuspids. This deposit (lead
sulphite) is always in the tissue outside of the blood vessels.
Plumbism causes trembling, nausea and vomiting. The patient
loses flesh, becomes anaemic, and has great resultant debility.

The lead circulating in the capillaries accumulates, owing to
impeded circulation resultant on a thickening of the coats of the
vessel, producing occlusion. A bluish line upon the gums indi-
cates that the system is completely saturated. Like mercury,
lead collects in the mucous membrane upon the inside of the
mouth, producing blue patches from a line to one-half an inch
in length. Lead not only produces local irritation, but affects
the peripheral nerves as well, producing trophic changes ; upon
the capillaries a thickening of the inner coat results in endar-
teritis obliterans. Brass produces, as Hogben 1 has shown, sim-
ilar effects to mercury and lead ; the green gum is an early
symptom.

Potassium iodide exerts a like toxic influence to lead and
mercury, as its pathology is similar thereto, but it is of infrequent
occurrence.

Scurvy is due to poor food and hygiene. Insufficient alter-
nation of food, impure air, want of bodily exercise, ennui and
uncleanliness combine the causes of this disease. Previous to
the introduction of canned goods, sailors on long voyages,
prisoners and others under confinement were subject to scurvy.
Lunatics, idiots or people who have had a long sickness, are now

1 Birmingham Medical Review, 1887.

NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 95

most prone to it. Anaemic convalescents from protracted fevers

suffer from it.

In the British Arctic Expedition of 1875-76 over forty-eight
per cent of the men suffered from scurvy. When the potato
crop tailed in Ireland, in 1846, scurvy became prevalent. In the
Crimean war 23,000 eases occurred among the French troops
alone. Scurvy contributed over fifteen per cent to the death rate
in the late civil war. It occurs among the Klondyke miners.

In public institutions fur degenerate children it is very
prevalent. I have observed it in both American and European
institutions.

Thomas Barlow 1 found scurvy associated with rachitis. Sun-
derland" found that rachitic diathesis was a very strong factor.
Jacobi reports forty cases of scurvy and rachitis. Babies in good
families brought up solely on the proprietary infant foods are
prone to scurvy. They lose their appetites, become pallid, per-
spire freely, have diarrhoea, the mouth becomes sore with inflamed
mucous membrane and gums. Purpura and haemorrhages of
mucous membrane are common with pain and swelling of the
joints.

In adults, excess of sodium chloride in the blood from con-
sumption of salt meats and fish has been noted with scurvy.
For this reason Rawls, of Cincinnati, Ohio, believed that an
excess of salt in the system produced gingivitis. Languor,
depression, amemia. with a rise of temperature, and enlarged
joints with soreness are the first symptoms.

The effects of this disease upon the system are almost identical
with those of mercury and lead. Bruise-like (purpuric) erup-
tions occur upon the skin and mucous membrane, on the serous
membrane (notably the pleura, pericardium, meninges and
synovial linings of the joints), mucous membrane of the mouth,
stomach, intestines and bronchi.

Owing to the anaemia, vascular weakness and altered compo-
sition of the blood, oedema is common both in the lungs and in
the submucous and subcutaneous tissue, especially the feet and
legs. The gums begin to swell with redness and fibrous thicken-
ing of the deeper layer, which cause protrusion, especially in

'Medical Chir. Trans., London, Vol. CXVI, 1883.
2 Practitioner, London, February, 1894.

96 INTEKSTITIAL GINGIVITIS.

the cases of degenerates. The blood vessels, especially the capil-
laries, become thickened, in some cases they are occluded, or ero-
sion and ulceration occurs. The patient becomes decidedly pale
and markedly debilitated. The skin is dry and blanched. Gen-
eral emaciation is evident.

The mucous membrane and gums become swollen and bleed,
stomatitis ulcerans results in greater or lesser degree. The
tongue is at first swollen, then it becomes dry and hard. The
gums are at first reel and swollen. They bleed easily upon the
slightest touch. Later they become pale and are irregularly
larger, somewhat fungoid and friable, protruding between the
teeth. They are quite tender to the touch. Ulcers appear on
the buccal surfaces. The stomach becomes irritable, nausea and
vomiting are common. Constipation occurs early and diarrhoea
later appears.

Factors acting through local trophic disturbances are not
-only local disorders but also constitutional diseases, especially
those which prevent elimination of effete matter (Bright's dis-
ease, diabetes, etc.) skin eruptions, lung affections, auto-intoxica-
tion (gout, etc.) and conditions like pregnancy, amenorrhcea,
dysmenorrhea, etc. The physiologic processes of nutrition,
growth and repair are regulated by local nerves which, as
already pointed out, because of this function are called trophic.
These are under control of both spinal and brain centers. Dis-
orders of the local nerve or of the higher centers may produce
trophic change. Such disorders affect more decidedly provi-
sional structures, since the growth, nutrition and repair of these
is normally unstable. The alveolar process is an outgrowth of a
permanent portion of the skeletal structure, provoked and main-
tained by the existence of what are really dermal appendages
and not true bones. It is a provisional structure, almost unique
of its kind in adult life, which has apparently little impendent
vitality. This is in part due to mechanical causes, since its
.slender structure unsupported by the teeth offers little resistance
to impacts from without, to which its situation renders it espe-
cially liable. There is more than this to be considered in reckon-
ing the special vulnerability of the alveolus. It is protected by
a thin layer of fleshy tissue only, which itself is peculiarly liable
to injuries, thus exposing the bone to infection. There is, more-

NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 97

over, no cavity of the body that is more open to germs than the
mouth, and some of these that arc considered ('specially viru-
lent are its constant residents. Access of germs and accidental
pathogenic factors to the alveolus is constantly afforded by cari-
ous teeth, the irritation of tartar deposits, etc. Its liability to
disease is thus indefinitely increased. As it is not very resistant
to morbid influences, the infections have thus free play, hence
suppurative disease is more readily induced.

Great practical importance, as Hirt ' remarks, must be attrib-
uted to the changes in the hair and teeth which are observed in
tabetics (locomotor ataxia). The teeth become loosened without
pain and fall out without appearance of inflammation ; the tooth
being seemingly intact. This Hirt ascribes to disturbance in the
nutrition of the jaw; an atrophic change connected with a lesion
of the nucleus of the trigeminus. The fact that this condition is
often connected with laryngeal crisis tends, in Hirt's opinion, to
support the view of Buzzard 2 that the center for bone nutrition
lies quite close to the vagus. Similar facts have been observed
by C. L. Dana in America. 3 The conclusion is obvious that dis-
turbance of the nerve centers governing nutrition, growth and
repair exerts the same influence on the alveolus, jaws and teeth
as similar disturbances do upon the skin, hair, mucous mem-
branes and bones elsewhere.

These structures, which have previously become affected by
disease, although the patient has been restored to health, readily
become the seat of interstitial gingivitis. This is illustrated in
those persons who have been affected with scurvy, salivation, etc.

1 Handbuch der Nervenkrankheiten, 1896.
2 British Medical Journal, February 19, 1886.
3 Diseases of the Nervous System.

CHAPTER X.

INTERSTITIAL GINGIVITIS IN DOGS.

The technique of the examinations of interstitial gingivitis
and pyorrhoea alveolaris in dogs was as follows : After fixing
and hardening in two per cent formalin, alcohol, or Muller's
fluid, the tissues were decalcified in a five per cent alcoholic solu-
tion of nitric acid, imbedded in celluloidin and stained in various
ways, the principal ones being hematoxylin and eosin. Ten or
more slides would be obtained from each tooth. Out of these
slides have been selected a series illustrating the progress of the
disease from beginning to the loosening of the tooth.

Fig. 31 is a longitudinal section of a cuspid tooth with the
alveolar process in situ. A illustrates the enamel of the tooth,
(E) the epithelium passes from the outer margin to the lower
border, then folds upon itself and extends down the side of the
crown of the tooth as far as the neck. Unfortunately, in this
specimen, the structure connecting the epithelium and the fibrous
tissue of the periosteum has been destroyed. The papillary layer
of the sub-epithelial tissue is plainly shown at the outer border.
Small round-cell inflammation may be seen extending along the
border of this layer. It can also be observed extending down
the capillary blood vessels into the submucous tissue (SI and G).

Fig. 32 shows a similar section of another tooth. Here the
epithelial structure (E) is pulled away slightly from the edge of
enamel (A). In this section the infolding of the epithelium is
shown at the neck of the tooth. This structure passes downward,
folds outward and upon itself (AA) and returns two-thirds of
the distance toward the gingival border, leaving a pocket (RR).
The epithelium (E) is very dense and thick. The papillary
layer of the submucous tissue (G) is very clearly defined. The
capillaries (K) can be distinctly traced from the deeper fibrous
tissue through the submucous layer into the papillary layer. The
thick and heavy fibrous tissue of the periosteum (" Dental Liga-
ment," Black) may be seen at H, inserted firmly into the

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 31. — Longitudinal Section of Tooth and Gum Tissue. Slight Gingivitis. Dog.

A, Enamel. E, Epithelial Tissue. G, Submucous Membrane. M, Fibrous Tissue
SI, Slight Inflammation.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced

Fig. 32. — Longitudinal Section of Tooth and Gum Tissue.
Gingivitis. Dog.

ne-third.
Chronic Interstitial

A, Enamel. E, Epithelial Tissue. G, Submucous Membrane. H, Periosteum.
K, Capillaries. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peri-
dental Membrane. RR, Space Pocket from want of Union of Epithelial Fold.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 33. — Longitudinal Section of Alveolar Process and Peridental Membrane. Slight
Interstitial Gingivitis, Extending into Alveolar Process. Dog.

J, Alveolar Process.

Inflammation Extending through Enlarged Haversian Canals.
I 1 , Inflamed Peridental Membrane.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 34. — Longitudinal Section of Alveolar Process and Peridental Membrane. Chronic
Interstitial Gingivitis, Extending into Alveolar Process. Dog.

H, Periosteum. J, Alveolar Process. V, Violent Inflammation. AA, Point of Union of
Epithelial Tissue and Peridental Membrane. I 1 , Inflamed Peridental Membrane. L 1 , Inflam-
mation Extending through Enlarged Haversian Canals.

INTERSTITIAL GINGIVITIS IX DOGS. 103

cementum and extending outward and downward. Just below
( AA) may be seen the interlacing of the coarser fibers of the peri-
osteum with the finer fibers of the submucous tissue. Chronic
round-cell inflammation may be seen extending from the papil-
lary layer through the capillaries into the interstitial tissue of
the submucuous layer and the periosteum. Marked inflammation
has occurred at Y. The openings in the folds of the epithelium
are fruitful sources for the accumulation of food, epithelial scales
and detritus, in which fermentation and decomposition from
micro-organisms result, producing inflammation.

Fig. 33 is a section through the peridental membrane (I) and
alveolar process (J) at the lateral incisor. The inflammation has
extended down from the papillary layer through the submucous
tissue, the fibrous tissue of the periosteum into the peridental
membrane and into the alveolar process. Round-cell inflamma-
tion may be seen in the blood vessels extending through the
Haversian canals (L 1 ).

Fig. 34 is a similar section from another tooth showing chronic
inflammation extending throughout the peridental membrane (I)
and alveolar process (J). The Haversian canals (L) are well
outlined by the inflammatory progress. Marked inflammation
has resulted at V and also at the margin of the alveolar process.

Fig. 35 is a section of the peridental membrane and alveolar
process, illustrating the effect of interstitial inflammation upon
the blood vessels and alveolar process. Chronic inflammation
extends throughout the peridental membrane with very decided
inflammatory change (V). The cut ends of the blood vessels
which were originally situated in the Haversian canals are seen
(BY). They have become involved with the result of a thicken-
ing of the walls and endarteritis obliterans. The bone about
these vessels has been entirely absorbed. The inflammation
has extended beyond, into and through the Haversian canals,
producing the type of absorption of the trabecular known as
halisteresis ossium. Lacunar absorption has also occurred (O).
Where decided inflammation (V) has taken place, abscesses are
more liable to occur (as will be noticed later) from the large
number of blood vessels at this locality.

Fig. 36 is a section from another location of the alveolar
process with a greater amplification, showing the inflammatory

104 INTERSTITIAL GINGIVITIS.

process extending through the alveolar process. Endarteritis-
obliterans may be seen in different localities (EO). Three forms-
of absorption are evident in this figure : Enlarged areas arising
from absorption of the trabecular (halisteresis ossium) due to the
inflammatory process. The vessels of Von Ebner precede perfo-
rating canal absorption (BB), distributed over the entire field, also
the result of the inflammatory process and lacunar absorption (O)
which may result from inflammation. As long as the fibrous tissue
remains in these large areas to retain the osteoblasts, new bone
tissue may be produced under favorable conditions. On the
other hand, when this tissue and the osteoblasts are destroyed, the
alveolar process cannot be restored.

Fig. 37 shows a section of the alveolar process from another
dog. Here lacunar and other absorption (halisteresis ossium) are
well shown. Thirty-seven osteoclasts (O) may be counted in the
field while destruction of bone by halisteresis (Q) is rapidly
going on. Remains of Haversian canals with the blood vessels
may be seen (BY, L). In the discussion of the peridental mem-
brane extending into the alveolar process (page 37), particular
attention was called to the fact that large bundles of fibers
extended into the process in such a manner as almost to isolate
portions of bone. In the lower left-hand corner (X) may be
seen two pieces of the alveolar process entirely separated from
each other and the main body of the bone. In interstitial gingi-
vitis, it is not uncommon to .find pieces of the alveolar process
separated by halisteresis and lacunar absorption. When loose
teeth are extracted as a result of this disease, pieces of the alveolar
process come away with the peridental membrane attached to the
tooth. Fig. 66 was obtained in this manner. In the upper left-
hand corner may be seen eight or ten new osteoclasts (O) in an
enlarged Haversian canal, at work isolating one piece of the
alveolar process from the other.

Fig. 38 shows a slide from still another dog. Halisteresis (Q)
and perforating canal (P) absorption are here well shown. In
the larger space at the lower left-hand corner may be seen two
arteries (EO) which were originally the location of Haversian
canals and which have thickened walls and a tendency to oblit-
eration. The light color shows decalcification, the dark normal
bone. At P may be seen perforating canal absorption. At FG

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 35. — Longitudinal Section of Tooth, Alveolar Process and Peridental Membrane.
Violent Round-Cell Inflammation of Peridental Membrane, Extending through the
Haversian Canals into the Alveolar Process.

C, Cementum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. N, Large
Spaces arising from Absorption of the Trabecule, starting in the Haversian Canals (Halistere-
sis). 0, Lacunar Absorption. V, Violent Inflammation. BV, Blood Vessels, originally Haver-
sian Canals. I 1 , Inflamed Peridental Membrane. L 1 , Inflammation Extending through
Enlarged Haversian Canals.

X 150. D. D. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 36. — Longitudinal Section of Alveolar Process. Chronic Inflammation Extending
throughout, showing h alisteresis, perforating c.\nal and lacunar absorption. dog.

J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecule, starting
in the Haversian Canals (Halisteresis). 0, Lacunar Absorption. P, Perforating Canal
Absorption. BB, Blood Vessels of V. Ebner preceding Perforating Canals. EO, Endarte-
ritis Obliterans.

X T.i. A. A. obj. Zeiss. Micro-photograph, reduced one-third.
Fig. 37.— Longitudinal Section of Alveolar Process. Chronic Inflammation Extending

THROUGHOUT, SHOWING HaLISTERESIS AND LACUNAR ABSORPTION. DOG.

J, Alveolar Process. L, Haversian Canals. N, Large Spaces arising from Absorption of
the Trabecular, starting in the Haversian Canals. 0, Lacunar Absorption. Q, Halisteresis
Ossium or Decalcified Bone. X, Remains of Calcified Bone. BV, Blood Vessels originally
Haversian Canals.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 38. — Transverse Section, Alveolar Process. Chronic Inflammation Extending
throughout. dog.

J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecule, starting
in the Haversian Canals. P, Perforating Canal Absorption. Q, Halisteresia Ossium or
Decalcified Bone. X, Remains of Calcined Bones. EO, Endarteritis Obliterans. FG, Fat
Globules.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 39. — Cross Section of Tooth, A lveolar Process and Peridental Membrane. Chronic
Inflammation of Peridental Membrane and Absorption of the Root of Tooth. Dog.

B, Dentine. C, Cementuni. D, Pulp. I 1 , Inflamed Peridental Membrane
S, Root-absorption.

K, Capillaries.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 40. — Longitudinal Section of the End of the Root of a Tooth, Alveolar Process
and Peridental Membrane, Showing Chronic Inflammation of the Peridental Mem-
brane. Exostosis of the Root of the Tooth and Lacunar Absorption. Dog.

C, Cementum. D, Pulp, with 3 Foramina. J, Alveolar Process. 0, Lacunar Absorption.
P, Perforating Canal Absorption. CC, Cementosis.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 41.— Cross Sectio.v of Inflamed Peridental Membrane. Dog.

II, Inflamed Peridental Membrane. \V, Epithelial Debris.

X 15. 75M.M.ot>j. Spencer. Micro-photograph, reduced one-third.

Fig. 42. — Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane,
Showing Interstitial Gingivitis and Pyorrhcea Alveolaris, with Tooth About to be
Exfoliated. Dog.

C, Cementuni. E, Epithelial Tissue. H, Periosteum. I, Peridental Membrane.
J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, Fibrous Tissue. R, Pus
Pockets. U, Nerve Tissue. V, Violent Inflammation. AA, Point of Union of Epithelial
Tissue and Peridental Membrane. CC, Cementosis. DD, Calcific Deposits Destroyed by Acids.

112

X -10. 35M.M. obj. Zeiss. Micro-photograph, reduced one-third.
Fig. 43.— Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane and
Gum Tissue, Enlarged from Fig. 42, Showing Active Inflammation, with Pis Pocket.
Dog.

C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. I 1 , Inflamed Peridental
Membrane. J, Alveolar Process. L 1 , Inflammation Extending through Enlarged Haversian
Canals. MMnllamed Fibrous Tissue. R, Pus Pocket. V, Violent Inflammation. AA, Point
of Vnion of Epithelial Tissue and Peridental Membrane. FF, Food Containing Micro-
organisms.

A. A. obj. Zeiss

ro-phototrraph, reduced one-third.

Fig. 44. — Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane and
Gum Tissue, Enlarged from Fig. 42, Showing Active Inflammation with Pus Pocket.
Dog.

C, Cementum. E, Epithelial Tissue. J, Alveolar Process. M 1 , Inflamed Fibrous Tissue.
R, Pus Pocket. V, Violent Inflammation.

INTERSTITIAL GINGIVITIS IN DOGS. 115

fat globules may be seen, while in the larger space at the upper
right-hand corner is evident entire destruction of the fibrous
tissue.

Fig. 39 Illustrates a cross section of alveolar process and
cuspid root, showing absorption of the, root. Inflammation
extends throughout the peridental membrane (I). The capil-
laries (K) are quite numerous. These are cut both crosswise and
lengthwise. Absorption (S) of the root may be seen progressing
at these localities.

Fig. 40 shows a longitudinal section of the end of the root.
Active destruction has been going on both in the pulp chamber
(D) and at the external surface of the cementum (C). The irri-
tation and inflammation has caused the odontoblasts to fill up the
pulp chamber with secondary dentine, and obliteration of the
chamber has taken place. Below the constricted pulp may be
seen three divisions of the pulp (D) extending through three
separate canals in the cementum (C). Cementosis ( CC ) may
be seen at the end of the root. Lacunar absorption is going on
(O ). Thus results a building up and tearing down of the same
tissue from the same cause, interstitial gingivitis..

Fig. 41 shows inflammation of the peridental membrane (I 1 )
with epithelial debris (W) scattered throughout the field.

Fig. 4_! is a section through the jaw and incisor tooth, showing
the relation of the structures to each other in a severe case of
interstitial gingivitis and pyorrhoea alveolaris. The tooth is
attached at only a very small portion of the apical end of the
root. The disease has been of long standing. Absorption of the
alveolar process on one side has progressed on fully one-half of the
root, while upon the other about one-third the distance. Inflam-
mation commenced at the gingival border and extended through
the periosteum (H), peridental membrane (I) and alveolar
process (J). Marked inflammation (V) has occurred in the
mucous membrane fold. An abscess has formed with a fistula
extending to the gingival border. The thin border at the left of
the fistulous tract is the epithelium layer next to the tooth. It is
evident that the pus burrowed to the surface through the struc-
ture instead of between the epithelium and the tooth. A similar
abscess and fistulous tract are evident upon the gingival border
on the opposite side of the tooth. The irritation produced by

116 INTEESTITIAL GINGIVITIS.

the movement of the tooth has caused the cementoblasts to
deposit large quantities of material upon the sides and the end of
the root. The main nerve trunks (U) may be seen at and below
the end of the root.

Fig. 43 illustrates the alveolar border on the right side of
Fig. 40, greatly amplified. This shows the progress of intersti-
tial gingivitis extending through the alveolar j)rocess producing
absorption with intense inflammation of the peridental membrane
and abscess with fistulous tract.

Fig. 44 shows a similar process amplified from the left side of
Fig. 42. It is interesting to note in this illustration that the
fibers of the sub-epithelium pass down and become interwoven
with the coarser fibers of the periosteum in just the opposite
direction from those in the other side of the tooth, and in other
illustrations. The fibers from the mucous membrane along the
side of the tooth extend down and into the peridental membrane
without a break in the structure. The arrangement of the fibers-
of the submucous layer in producing the fold is well illustrated
in the figure. This picture illustrates inflammation starting in
the gingival border.

CHAPTER XI.

MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS.

To secure a chain of evidence that interstitial gingivitis (due
to the metals, drugs, uric, lactic and other acids) commenced in
the papillary layer of the sub-epithelial, mucous membrane, I
instituted a series of experiments in mercurialization of dogs.

Proj. ' 4 inch, ocular IS inch. Spencer.

Fig. 45. — Longitudinal Section of Gingival Border, Showing Round-Cell
Inflammation Due to Mercurial Poisoning.

Dogs for the purpose were picked up in the streets. Some
of these were operated upon by myself, but most of them were
under treatment at the Post-Graduate Medical School. Care
was taken to secure those in health and with healthy gums.
Mercury was introduced by the mouth, skin and hypodermic

118

INTERSTITIAL GINGIVITIS.

injection. It was no easy matter to get them under influence
of the drug, since the power of the glands to eliminate the poison
was enormous. In no case was salivation produced. The first
symptom noticed was exhilaration, which would last from three
days to a week. Then paralysis agitans would continue until
death. In about a week the appetite would commence to fail
and it was difficult to get the dogs to take food of any kind.
The kidneys and bowels eliminated the poison. There was a

Pantachr

■)] ocular. No. 3. Leitz.

Fig. 46.— Longitudinal Section ok Gingival Border. Higher Magnification,
Showing Connective Tissue Infiltration with Plasma Cells and Polynu-

CLEAR LeUCOSYTES. DOG.

rise in temperature. Some of the dogs died before gingivitis
was observed. This demonstrated that not only does the nervous
system become involved, but the organs of the body may be
morbidly affected and death ensue before the gums show symp-
toms of disease. Some dogs were killed after the gums became
diseased. The time required to obtain results was from three to
eight weeks. The age and physical condition of the dog caused

MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS

lit.)

this variation in time. After death the gum tissue was dissected
from different parts of the jaws and placed in either fifty per
cent alcohol, Miiller's fluid, or two per cent formalin.

Sections of tissue from the gum margin and sides were made
on a number of places. Some were imbedded in paraffin, others
in celluloidin. The sections were stained according to various
methods: Delafield's hematoxylin, eosin (Unna's), alkalin
methylblue, carmin, Gramm's stain, etc.

Fantachr. oil 1mm. ,'., inch ocular. No. 3. Leitz.

Fig. 47. — Longitudinal Section of Gingival Border. Higher Magnification,
Showing Round-Cell Inflammation Extending to the Inner Coat of the
Blood Vessel and also Plasma-mast Ceils.

Microscopic examination showed that the epithelial lining of
the gums did not present pathologic changes, but appeared
normal in every respect. Connective tissue below the gum
epithelium (the tissue analogous to the papillary layer of the
derma and the derma proper) presented unmistakable evidences
of a mild inflammatory process. There occurred in this con-
nective tissue round-cell infiltration, generally moderate hut in

120 INTERSTITIAL GINGIVITIS.

some places quite dense. This cellular infiltration extended
from below (where it was densest) upward into the papillary
layer (Figs. 45 and 46). The densest cellular infiltration
usually occurred around the vessels (Fig. 46).

Under high magnification, the cellular infiltration was found
to consist of polymorphonuclear leucocytes, plasma cells and

Projection U inch, ocular l'/ 2 inch. Spencer.

Fig. 48. — Longitudinal Section of Gingival Border, Showing Round-Cell Infil-
tration in the Connective Tissue and Extending into the Papill.e. Dog.

plasma-mast cells, the latter with coarse basophilic granulations
(Figs. 47 and 48).

In some places were seen between the round cells, short,
broad fusiform cells, the protoplasm of which took quite well
basic methylblue. These cells resemble very much fibroblasts
and appear to be derivations of the plasma cells (Fig. 49). No
bacteria were found either in the areas of cellular infiltration
(inflammatory areas) or elsewhere. In these cases it is obvious
that there had occurred a mild inflammation of the gums (gingi-

MERCURIAL INTERSTITIAL GINGIVITIS IX DOGS.

121

vitis). While this could not be seen with the naked eye,
microscopic examination demonstrated histologic features of an
inflammatory process. The absence of bacteria justified the
belief that this inflammation was not of microbic origin, but due
to mercury, which by its well-known chemotactic influence pro-
duced the histologic changes of an inflammation.

Pantachr. oil imm. ( ' a inch ocular. No. 3. Leitz. •

Fig. .49. — Longitudinal Section of Gingival Border, Showing Round-Cell
Inflammation Due to Mercurial Poisoning. Higher Magnification.

CHAPTER XII.

BACTERIOLOGY OF INTERSTITIAL GINGIVITIS.

The bacteric etiology of interstitial gingivitis has been inci-
dentally discussed by many writers.

Galippe 1 was probably among the first to make analytic
experimentation in the bacteriology of this disease. He claims
that there is found in the pus of pyorrhoea a parasite, resembling
in shape the Greek letter N. Injecting this into the belly of a
guinea pig, abscesses resulted, which had a special tendency to
affect I tone tissue. Injections into the sjmce between the teeth
and gums were negative in result. Galippe regards his experi-
ments as suggestions for further research, but not demonstra-
tive. Miller, 2 after explaining his own methods, made a series of
culture experiments on agar-agar at blood temperature. Twelve
cases of pyorrhoea in human beings, and six in dogs, were exam-
ined. He isolated twenty different bacteria from human beings,
and nine from dogs. Among the twenty kinds, staphylococcus
pyogenes aureus was found twice. Staphylococcus pyogenes
albus once, streptococcus pyogenes once. Of the other sixteen,
nine subcutaneously injected produced no particular reaction,
four a slight, three a severe suppuration in the subcutaneous con-
nective tissue Among the nine species found in

■dogs, staphylococcus pyogenes albus occurred once. Of the
other eight, two subcutaneously injected caused no reaction, and
five but slight. One caused very profuse suppuration, by which
large portions of skin exfoliated Microscopic exami-
nation of stained sections revealed masses of different bacteria,
cocci and bacilli. Leptothrix occurred infrequently, and then
■only on the surface of the cement, and where there were micro-
scopical cavities in it Miller succeeded consequently

in cultivating a large number of bacteria from pyorrhoea alveo-
laris which possessed pyogenic properties, but was not able to

Die InfectiiJse Arthro-Dentiiire Gingivitis, 1888.
Micro-Organisms of the Human Mouth.

BACTERIOLOGY OF INTERSTITIAL GINGIVITIS. 123

determine the constant occurrence of any one which might be
regarded as the specific micro-organism of pyorrhoea alveolaris.
Miller remarks that it is not evident from Galippe's communica-
tion whether he found the N or /S bacterium in all cases exam-
ined, or hut once.

Sudduth, after repeated examinations, arrived at the same
conclusion as Miller.

The results obtained in the Columbus Memorial Laboratory
of Chicago, by W. A. Evans, were as follows:

In order to determine whether a specific bacterium existed in
the pyorrhoeic stage of interstitial gingivitis in man (necessary
to constitute this stage a special disease), pus from more than fifty
cases was examined. In all, the pus was obtained from the gums
by a platinum needle under proper methods of sterilization. The
pus from some cases was smeared on a slide. This was stained
and such determination made as was possible with this proce-
dure. With the pus from fifteen cases, agar was inoculated and
placed in Petrie's dishes. The individual colonies were grown
on gelatin, agar, bouillon, potato and blood serum. The results
were as follows: In fifteen cases in which the organisms were
plated out, fifty-five organisms were found. In two there was
no growth. Two had but one species of germs, two had six, one
had seven, and one had ten. The germs found are divisible into
three classes: Those usually pathogenic to man, those excep-
tionally pathogenic to man, and those never pathogenic to man.
The first class was found thirty times, the second twelve, and the
third thirteen. Class third is, no doubt, seemingly smaller than
it should be, since many members of it probably do not grow on
ordinary culture media. Of the germs most frequent ami
important, staphylococcus pyogenes aureus occurred nine times,
staphylococcus pyogenes albus six times, and staphylococcus
pyogenes citreus once. A lanceolate diplococcus, growing like
pneumonococcus, was found six times. Streptococcus pyogenes
was found twice. Bacillus coli commune was found twice. A
bacillus growing like the diphtheria bacillus occurred twice.
This last bacillus had the appearance of the Kleb-LoefhVr bacil-
lus. It lav on the slide like it and it stained irregularly. Of
the less important organisms - , bacillus pyocyaneus was found three
times, micrococcus tetragenus seven times, leptothrix seven times,

124 INTERSTITIAL GINGIVITIS.

bacillus mesentericus twice, bacillus subtilis three times. There
was also present a peculiar large club-shaped fungus somewhat
resembling the degenerative forms of actinomycosis.

Did these examinations stand alone, definite conclusions could
not be drawn from them. These, however, are admissible since
all observations on this subject tend in the same direction.
While, as already stated, Galippe believed that he had isolated
two bacteria capable of causing pyorrhoea alveolaris, still he
failed with both to produce the disease. This failure, according
to the laws of Koch, is fatal to the position taken.

M. Herzog, of the Chicago Polyclinic, on examination of
cases of interstitial gingivitis, which had not reached the pyor-
rhceic stage, had the following results : Pieces from the gum mar-
gin which had been fixed and hardened in a formalin solution,
were partly imbedded in celloidin, partly in paraffin. The sec-
tions were stained according to various methods, including
Gramm's, eosin (Unna's) and alkaline methylblue stain. The
examination of the tissue shows an unchanged lining of stratified
squamous epithelium, aud, in the connective tissue below the
former, well-marked evidences of an inflammatory process. The
round-cell infiltration is best marked in the deeper layers toward
the periosteum, while the layers of connective tissue fibers nearer
to the lining epithelium show less evidences of inflammation and
are partly entirely free from any round-cell infiltration. The
infiltrating round cells are of the type of lymphocytes, plasma
cells and plasma mast cells. Very large and typical mast cells
'are frequently found in the neighborhood of small vessels.
Many of the vessels seen are quite tortuous, and the vascular sup-
ply of the connective tissue appears to be considerably increased
beyond the normal. Bacteria could not be demonstrated in the
inflamed areas.

M. Herzog's examination of the interstitial gingivitis, pro-
duced by mercury in dogs, failed to reveal any bacteria. He was
of opinion that the histologic changes of inflammatory type
found, were due to the chemotactic influence of mercury and not
to microbic action.

In a paper 1 read before the Section on Stomatology of the

'Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhoea
Alveolaris.

BACTERIOLOGY OF INTERSTITIAL GINGIVITIS. 125

American Medical Association, at Columbus, Ohio, George T.
Carpenter mentioned some very interesting experiments in this
connection. By infecting a fresh wound in the gums of rabbits
with pyorrhoea and other pus he found the parts will remain
infected only from two to five days. In other rabbits a rubber
band was placed around teeth and pressed under the gums until
inflammation resulted, when the parts were infected with pyor-
rhoea and pus from a chronic ulcer; pus infection resulted.

Like experiments were made in the human mouth on gums
which had been neglected as well as on healthy gums, and with
similar results. His experiments tend to show that, when animals
and man are healthy, the tissues resist infection ; but when
diseased, infection results. All yield to treatment.

On examination of pus taken from pyorrhoea, pockets pro-
ceeding from acute infection, two competent bacteriologists were
unable to find a micro-organism not found in pus from other
infected tissues.

These results, in Carpenter's opinion, tend to show that a
specific germ, to which pyorrhoea alveolaris is attributable, has
not yet been found.

The disease being so prevalent among dogs, it occurred to me
that they would be of great value for experimental inoculation.
The prevalence of the disease in dogs suggests that if it were a
specific infection, these must be inoculable. Miller 1 had made a
few inoculations of pus as well as of the deposits around the
teeth. Slight inflammation, and, in one case, a little suppuration
alone resulted. He afterward isolated twenty different bacteria"
from the human mouth and nine from dogs. Some of the
uncommon varieties were infective, but without marked results.
Isolated varieties would probably not produce results that could
be attained by inoculating animals with the fresh secretion (pus
and other deposits) from dogs already affected with the disease. A
dog was procured from the Veterinary Hospital whose gums and
outer alveolar process w r ere almost entirely absorbed with pus
exudate. Street dogs selected for inoculation were forty-six in
number, ranging in age from one year to seven. They were of
all breeds and conditions. Some were well fed, others very thin.
Many had sound, healthy gums ; others had slight inflammation

1 Miero-Organisms of the Human Mouth, page 329

126 INTEESTITIAL GINGIVITIS.

at different localities. No dog was used whose gums and alveolar
process had become infected or whose tissues were absorbed. Two
dogs were operated upon at a time. The gum was separated from
the necks of the teeth down to the alveolar process and peridental
membrane — one half at the canine, the other at the second
pre-molar, since in a majority of cases the disease began at the
canine tooth, probably on account of its prominence and the
thinness of the alveolar process. The second pre-molar was
selected because it is the least prominent. The secretions about
the teeth and gums of the diseased dog were collected upon
a platinum wire (previously sterilized) and conveyed to the
injured parts. Thirty-nine healed in eight days. In these
the gum tissues were healthy. The pus had no effect. The
wounds healed as rapidly as any wounds possibly could. In
seven the gums were inflamed and infection occurred. Suppura-
tion was slight in four and considerable in three. The patho-
logic findings in these cases were not unlike inflammation and
infection in other tissues. Similar results would, no doubt, have
taken place if inoculation had been performed with pus from an
abscess. The last three dogs were allowed to depart at the end
of four weeks with slight pus infection.

CHAPTER XIII.

SCORBUTIC INTERSTITIAL GINGIVITIS IN MAN.

While hundreds of slides could be adduced in support of this
chain of evidence, sufficient have been given to permit of the
introduction of evidence from other phases of the subject.

The following- autopsy was made by L. Hektoen on an old
man, in whose case the pathologic diagnosis was as follows :
Senile marasmus (senile emphysema, senile sclerosis of the aorta,
atrophy of the parenchymatous organs), scurvy (hemorrhagic
gingivitis ) ; chronic aortic and mitral endocarditis ; fibrous
myocarditis; chronic nephritis; caseo-calcareous areas in the
right apex, spleen and left adrenal; double hydrothorax; bron-
chitis ; fibroma of the stomach ; amputation of the left lower
extremity at the lower third of the thigh. The findings unre-
lated to the scope of the present investigation are omitted. The
gums were found swollen, and here and there infiltrated with
blood. There was purulent matter about the roots of the teeth,
many of which were loosened and some of which could be
removed with the fingers. The roots of the loosened teeth were
covered with a granular grayish material.

Bacteriologic examination of the root of the tooth gave the
following results : Tube of bouillon from which agar plates
were made, inoculated twenty-four hours before date, July 29,
1898. There were two varieties of colonies: Both grayish white.
One kind is round, pin-head size, slightly elevated, with thin,
wavy, but sharply defined border. Finely granular. Media
inoculated from one of these. Agar Slant: White, tallow-
like growth along the track of the needle, with thin, more trans-
lucent layer covering the rest of the surface. ( )nlv moderately
elevated. Greenish tinge given to media. Potato: Elevated,
"clumpy" growth, while on top, confined to needle track.
Potato much darkened. Blood Serum: Gray, waxy growth,
little elevated, sharply defined and thick border. Gelatin Slab:
Saucer-shaped Liquefaction at upper part, more tubular in deeper

128 INTERSTITIAL GINGIVITIS.

portions. Flocculent masses throughout. Glucose Agar: Gas
produced, white, thick growth on top. Milk: Alkaline, soft
coagulation. Bouillon : Cloudy. Characteristics : Rapid growth,
a sour, nauseating odor given off from all media, Morphology :
Large coccus, single, in pairs and in groups. Stains easily by
ordinary methods, also by Grams. The smaller colonies on agar
plates (pin-point sized in center) with nearly transparent, illy
defined peripheral zone. Border indistinct. Central portion in
gray. Finely granular throughout. Agar Slant : Gray film
over entire surface, somewhat thicker along the inoculation streak.
At bottom there is a nearly white growth. Very light, greenish
tinge to media. Blood Serum : Like on agar. Potato : Heavy
dirty gray growth, wavy and sharply defined border. Looks like
bunch of cauliflower. Gelatin Slab : Liquefied, saucer-shaped
at top, tubular in deeper part. Growth mostly in upper stratum.
Lit. Milk: Negative. Bouillon: Cloudy. Glucose Agar:
Gas produced. Characteristics : Rapid growth, stinking odor
from all media. Morphology : Small, slender bacilli ; actively
mobile, spores. Takes ordinary stains readily and is not decol-
orized by Gram's method.

Only the lower frontal teeth and corresponding part of the
jaw could be examined. The epithelial covering of the gums
appeared to be quite intact. In some places it was a little thick-
ened, and its lower layers infiltrated with new cells. The sub-
epithelial tissue was much thickened, presenting the general
structure of an inflammatory granulation tissue of some stand-
ing. Areas occurred in which there were many new cells and but
little stroma. In other foci the tissue was more fibrous, the new
cells running in bands. Here and there occurred free and
intracellular granular, yellow pigment, Typical hyaline bodies
of various sizes, and staining a precise bluish violet with Gram's
method, were found in rather small numbers. In some places
small sub-epithelial abscesses were met with, which (in the instance
of a district including a lower incisor) were really subperiosteal.
The contents consisted of nuclear detritus and bacteria (mostly
cocci) which have accumulated, especially upon and in the walls
of the minute cavities extending from such an abscess. There
seems to be a complete occlusion of the vessels (capillaries) with
typical bacteria masses, staining a peculiar bluish violet color

X 40. 35 M.M. Zeiss. Micro-photograph, reduced one-third

Fig. 50. — Longitudinal Section of Tooth, Alveolar Process and Gingival Border,
Showing Active Inflammation in Scurvy in Man.

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane.

H, Periosteum. J, Alveolar Process. L, Haversian Canals. M, Fibrous Tissue. V, Violent

Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Membrane.
RR, Space Pocket from Want of Union of the Epithelial Fold.

:::. MM. Zeiss.

photograph, reduced one-third.

Fig. 51. — Longitudinal Section of a Tooth, Alveolar Process and Gingival Border,
Showing Active Inflammation in Scurvy in Man.

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. V, Violent
Inflammation. Z, Sloughing of the Epithelial Tissue Due to Calcic Deposits. AA, Point of
Union of Epithelial Tissue and Peridental Membrane.

A. A. obj. Zeiss.

iluri'il ont'-thivil.

Fig. 52.— Longitudinal Section of Tooth, Alveolae Process and Peridental Membbane,
Showing Blood Pigment in Blood Vessels of Peridental Membbane in Scurvy in Man.

C, Cemenlum. J, Alveolar Process. K, Capillaries. I 1 , Inflamed Peridental Membrane.
K 1 , Blood Pigment in Capillaries.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 53.— Longitudinal Section of Tooth and Gingival Boeder, Showing Active Inflam-
mation Extending through the Mucous and Peridental Membranes. Scurvy in Man.

B, Dentine. C, Cementum. E, Epithelial Tissue. V, Violent Inflammation. AA, Point
of Union of Epithelial Tissue and Peridental Membrane. RR, Space Pocket from Want of
Union of Epithelial Fold. M 1 , Inflamed Fibrous Tissue.

SCOEBUTIC INTERSTITIAL GINGIVITIS IN MAN. 133

with hematoxylin, and bine with Gram's method, so that the
vessels presented the appearance of being very successfully filled
by an infection mass : the small dilatations, the branches and the
larger vessels (judging from structure these seemed to be veins)
were sometimes brought out very nicely. The intravascular
growth of bacteria extended into the bone below as well as, and
more especially into, the peridental membrane. 1 These abscesses
(suppurative periostitis) occur almost exclusively upon the inner
surface of the alveolar process, being confined (as far as there
was occasion to observe) to the external aspect of the process.
There was always a thin, sound layer of bone separating the
abscess from the peridental membrane. Very generally the
spaces in the adjacent bone were filled with a cellular fibrous
tissue in which occurred islands of osteoid tissue. The bone
trabecule were generally covered by a thin layer of osteoid
tissue, which (from the greater number of cells it contains, as
compared with the other bones) must be newly formed. Rows of
osteoblasts were found often upon the trabecule. Few How-
ship's lacunae were found, and these were filled with small cells.
There were no osteoclasts in the areas about the abscesses. The
bone outside of the alveolar process is quite unchanged.

The " bacterial thrombosis " not unusually extended into the
peridental membrane, which then refused to stain as clearly as
normal. The upper part of the peridental membrane was
usually the seat of cell proliferation, and of the formation of
fibrous tissue, due to the direct extension of the similar process
in the sub-epithelial connective tissue of the gingivus. There
were no indications that the process began below, at the apex of
the tooth, for example, and extended upward. In the peridental
membrane, and often connected with the cementum of every tooth
examined, were very many so-called calcospherites ; calcified,,
concentrically lamellated, round or oval bodies, not unlike the
" corpora amylacea." In many instances, it seemed as if the
body had formed in the cement or at its margin — the cement
presenting here a nodular condition.

Fig. 50 illustrates a section through the tissues of the jaw

1 The abscesses have a definite outline or wall of ordinary cellular fibrous tissue
displaying striking evidences of active inflammation. The tissue about the capilla-
ries filled with bacteria refuse to stain clearly, but there are no signs of inflammation.

134 INTERSTITIAL GINGIVITIS.

and cuspid tooth. The epithelium is not so dense and thick as.
in a similar section from the dog. Inflammation extends along
the papillary layer of the submucous membrane (G) and involves
the deeper structures. The mucous membrane layer has doubled
upon itself, forming a pocket (R R). Violent inflammation is
evident at A". This is of unusual interest, since it demonstrates
that inflammatory products may be carried by the blood vessels
anywhere throughout the alveolar process, and may result in
abscesses. The inflammation extends throughout the periosteum
(H), the fibers of which extend from the root of the tooth over
the border of the alveolar process (J). There the coarse fibers
of the periosteum contrast decidedly with the finer fibers of the
sub-epithelium. Absorption and contraction of the alveolar pro-
cess (fully one-half the length of the root of the tooth) has taken
place, as well as lateral absorption. The inflammatory process
extends through the Haversian canals (L).

Fig. 51 is a section through the jaw at the lateral incisor.
The epithelium (E) is seen upon the outer surface of the alveolar
process as far as the root of the tooth. The inner fold next to
the tooth has disappeared through encroachment of deposits
which have been destroyed by nitric acid. Inflammation
extends throughout the entire submucous membrane (G). The
most marked inflammation in this case is entirely upon the
outer border (V).

Fig. .12 shows a section of the peridental membrane (I)
and alveolar process (J). Capillaries (K) interlace through
the field, the largest number being distributed along the
alveolar wall. Blood pigment containing bacteria are notice-
able (K').

Fig. 53 is an amplification of a section depicted in Fig. 50.
This gives a clearer idea of the folding of the epithelium (E)
and submucous membrane (G) layer upon itself, forming a pocket
(RR), in which may be seen an accumulation of food and
bacteria. It also shows extensive inflammation throughout the
entiie field. Marked inflammation is evident at V. The point
of union of the sub-epithelial layer and the periosteum is shown
(AA).

Fig. 54 illustrates inflammation of the peridental membrane
with epithelial debris (W) scattered over the field, Endarteritis

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 54. — Cross Section Peridental Membrane, Showing Active Round-Cell Inflamma-
tion. Scurvy in Man.

C, Cementum. V, Violent Inflammation. \V, Epithelial Debris. EO, Endarteritis Obliterans.

Fig. 55.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.
-Cross Section of Inflamed Peridental Membrane. Scurvy in Man.

I, Peridental Membrane. J, Alveolar Process. K, Capillaries. L, Haversian Canals.
BB, Blood Vessels of Von Ebner Preceding Perforating Canals. EO, Endarteritis Obliterans.
W, Epithelial Debris.

x ;."i. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 56. — Cross Section of Tooth, Alveolae Process and Peridental Membrane, Showing
Active Inflammation cnd Absorption of Bone. Scurvy i\ M w.

C, Cementum. I, Peridental Membrane. J, Alveolar Process. P, Perforating Canal Absorp-
tion. V, Violent Inflammation.

X 40, 35 M.M. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 57.— Cross Section of Peridental Membrane and Alveolar Process, Showing Active
Inflammation and Abscess. Scurvy in Man.

Alveolar Process. T, Bacteria. Y, Abscess. I 1 , Inflamed Peridental Membrane.
L, Inflammation Extending through Enlarged Haversian Canals.

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third.

Fig. 58. — Cross Section of Peridental Membrane and Alveolar Process, Showing Active
Inflammation and Another Larger Abscess. Scurvy in Man.

J, Alveolar Process. P, Perforating Canal Absorption. V, Violent Inflammation.
Y, Abscess. I 1 , Inflamed Peridental Membrane. L 1 , Inflammation Extending tbrougb Enlarged
Haversian Canals.

I Mil

140

1 NT E RST I T I A L GI XGIVITIS.

obliterans (EO) is also noticed at various positions. Marked
inflammation may be seen at V.

Fig. 55 illustrates a section of the peridental membrane (I)
and alveolar process (J) with inflammation extending through-
out. Capillaries (K) are also noticeable in large quantities,
nearer the alveolar process than the root of the tooth. Epithe-
lial debris are evident at W. Endarteritis obliterans (EO) may

X 300. No. 2 projection ocular. D. D. obj. Zeiss.

Fig. 59. — Cross Section of Tooth, Alveolae Process and Peridental Membrane, Showing

Active Inflammation with Calcospherite in Membrane. Scurvy in Man.

B, Dentine. C, Cernentum. I, Peridental Membrane. J, Alveolar Process. HH, Caleo-
spherite. J', Inflamed Peridental Membrane. L 1 , Inflammation Extending through Enlarged
Haversian Canals.

be seen in different portions of the field. Inflammation has
extended into the Haversian canals (L) but absorption has not
occurred to any great extent. The blood vessels of Von Ebner
(BB) are quite well shown.

Fig. 56 is a section showing the cernentum (C), the peri-
dental membrane (I) and the alveolar process (J). Marked

SCORBUTIC INTERSTITIAL GINGIVITIS IN MAX. 141

inflammation extends through the peridental membrane, thence
through the Haversian canals ( which are entirely obliterated ).
Absorption of the trabecular (halisteresis) lias resulted to the

extent that what remains of the alveolar process (J) are islands
of bone held in place by the fibrous tissue. Blood vessels of
Yon Ebner with perforating canals are seen at P.

Fig-. 57 shows a section of the peridental membrane and
alveolar process with a large abscess originally within the
alveolar wall. Inflammation spreading through the peridental
membrane has occurred at I', while the decalcified alveolar
jjrocess is also shown (J). Violent inflammation has taken
place within the alveolar wall, and an abscess ( Y) has formed.
The wall of the ;d>sce<s is distinctly seen, with masses of bac-
teria ( T ) clinging to the inner sides. The process of halisteresis
(Q) (hone decalcification) is seen as a result of the violent
inflammation. The entire wall next to the peridental membrane
and about the abscess has been destroyed, and the different stages
in the process by which this has been accomplished are beauti-
fully shown.

Fig. 58 illustrates a larger abscess (Y) from another loca-
tion. This is also situated within the alveolar wall, showing
that the inflammatory products extend through the blood ves-
sels. Marked inflammation i> seen upon the side next to the
peridental membrane (I'), while rapid absorption — halisteresis
(Q) and perforating canal (P) — is proceeding at the borders
of the abscess and nearest the alveolar process.

Fig. 59 shows a section of a tooth (B and C), inflamed
peridental membrane (I'), with absorption of the alveolar pro-
cess {,]). In the inflamed peridental membrane may be seen
a calcospherite. oblong in form.

CHAPTER XIV.

INTERSTITIAL GINGIVITIS IN MAN FROM DRUG ACTION.

A forty-eight-year-old merchant was dyspeptic, debilitated
and asthmatic, and for the treatment of these conditions he had
been under calomel and tonics for a little less than two weeks.
When he came under observation, the mucous membrane and gums

were then much inflamed. There was marked sialorrhcea. The
teeth were loose. The gums were swollen. Pus oozed from the
gums. The breath had a decided metallic odor. At my sugges-
tion, his medical attendant stopped the calomel. He was then
ordered six pints of spring water daily. The gums were, on
alternate days, saturated with iodin. In a few days the soreness
and swelling were so reduced that the deposits could be removed.
The patient was discharged cured in a short time other than as to
the right inferior second molar, which was so loose as to require
removal. This tooth was placed immediately in fifty per cent
alcohol for twenty-four hours and then removed to absolute

INTERSTITIAL GINGIVITIS IN MAN

FROM DRUG ACTION. 143

alcohol for twenty-four hours more. The membranes had
receded about two-thirds the length of the root. Sections for
microscopic purposes were made from the lower third of the root.
Of these sections, Fig. 60 shows a small fragment of inflamed
peridental membrane. Fig. 61 exhibits violent round-cell inflam-
mation, degeneration and liquefaction of tissue.

A thirty-five-year-old diabetic painter came under observation
for plumbic poisoning. His gums were swollen. There was
decided sialorrhoea. The teeth were loose. Pus flowed from the

Fig. 61.

gums. He was placed on ozonate spring water and the gums
were saturated with iodin on alternate days. Three loose teeth
were removed and placed in alcohol. Sections from the upper
third of the left superior second bicuspid gave results on micro-
scopic examination similar to those already described as occurring
in mercurial poisoning. Fig. 62 sIioavs round cells of inflamma-
tion. Fig. 63 illustrates very marked degeneration of the peri-
dental membrane. In the lower right-hand corner are seen the
root of the tooth, dentine and cementum. The whole surface of

144

IXTEKSTITIAL GINGIVITIS.

the peridental membrane is in an advanced phase of inflamma-
tion. Just at the border of the root is evident an area of mem-
brane softening. Just beyond, but joining, is noticeable breaking
down of tissue. In the center are seen two areas of softened
tissue more advanced in degeneration.

One occupation disease which has been ignored in the etiology
of interstitial gingivitis is "brass-workers' ague." In almost all
brass-workers, a stain varying from a bright to a brownish green
is detectable on the necks of the teeth between the crowns and
the gum insertion. This is most obvious in the upper jaw.
After a while, as E. Hooben 1 has shown, the teeth become

loosened and fall out, Before these changes in the gum occur
nervous symptoms have developed from the brass poisoning.

Arsenic should be taken into account in the etiology of inter-
stitial gingivitis. This drug has a very decided tendency in cer-
tain subjects to cause, even in small doses, marked stomatitis and
irritation of the mucous membranes throughout the body.

Tartar emetic and the other preparations of antimony, produc-
ing irritation of the mucous membranes of the mouth and else-
where, may act as predisposing and exciting factors of interstitial
gingivitis. 2

1 Birmingham Medical Review, 1887.

2 Lewin : Untoward Effects of Drugs.

[NTERSTTTIAL GINGIVITIS IX MAX FROM J>I!1

145

Among the drugs which should be taken into account in the
etiology of interstitial gingivitis is potassium bromide. This
produces in certain individuals, or when given to excess, marked
increase of the saliva with irritation of the mucous membranes
of the mouth, followed later by dryness of the mouth and shrink-
ing of the gums. The bromides have, as II. C. B. Alexander 1
has shown, a tendency to irritate all the mucous membranes of
the body as well as the skin. Therefore, in dealing with cases
of interstitial gingivitis in which the bromides are being taken,
this factor should not be neglected. In these cases the symptoms

Fig. 63.

due to the bromides are apt to he charged to the nervous state for
which the bromides have been given. The irritation of the
mucous membrane by the bromides may occur quite early among
the untoward effects produced by them. In all probability the
bromine rather than the alkali is the source of these untoward
effects.

What is true of the bromides is also true to an even greater
degree, as has elsewhere been shown, of the iodides.

1 Alienist and Neurologist, July, 1890.

CHAPTER XV.

CONCLUSIONS.

While, as already shown, the teeth originated in the epider-
mis, still, even as early as the sharks, the teeth of the mouth
departed from this primitive method of development, since they
did not arise on the surface, but deep down, as Minot 1 has
pointed out. As Hertwig has shown, this occurs because the
dentiferous epithelium grows down into the dermis, forming an
oblique shelf, which may be regarded as a special tooth-forming
organ. On the under side of the shelf the teeth are developed
in the same way as over the skin, although they are much larger.
The teeth are, however, in various stages of development, and
only one is fully exposed ; when, as happens in time, it is lost,
the next tooth behind replaces it. Since the production of new
tooth germs goes on in adult life, replacement of the tooth in the
shark's jaw continues indefinitely; hence sharks are termed
polyphyodont. Mammals, having two sets of teeth only, are
called diphyodont. There is, therefore, even in mammals where
the change is limited, a tendency to change. Since the human
being and the higher mammals (noticeably the omnivora, like
dogs, whose food is as varied as that of man) are born practically
toothless, this struggle begins between the teeth at a later time
than in the lower vertebrates.

The teeth are temporary structures, intended to be shed at
certain times ; the temporary set ere the onset of jmberty, the
permanent with the onset of senile involution at the premonitory
period of old age. This last period depends on the individual
rather than the number of years lived. At the senile period,
which may occur at any time after the eruption of the perma-
nent set, osteomalacia (which is the normal absorption of the
alveolar process) may take place. The period at which this
commences depends upon the constitution of the patient,
Through congenital defect or disease, senility may begin earlier

1 Human Embryology.

CONCLUSIONS. 147

iii life. In certain types of degeneracy ( precocity, for example),
senility with absorption of the alveolar process may begin even
at twenty. Absorption of the alveolar process and loss of the
permanent teeth, is, therefore, certain at a period dependent
upon the constitution of the patient. Between these two periods,
birth and senility, two sets of teeth have been furnished man.
In the meantime, the alveolar process, the gums, periosteum,
peridental membrane, blood vessels, nerves, have come and gone
to suit the convenience of these two sets of teeth. Tissues Like
these are called adventitious or transitory. Adventitious tissues
are much more apt to be affected by disease than permanent in
type and persistent in function.

As transitory structures, destined to fulfill temporary pur-
poses, the teeth of necessity tend to decrease in number with
advance in development for the benefit of the organism as a
whole, thereby preventing waste of nutriment on useless struc-
tures. The shapes of teeth hence vary in order to adapt them-
selves to the work and surroundings produced by evolution.
The teeth and its setting being of different structures and com-
position, each proceeds to destruction along lines imposed by the
laws of its structure. The tooth is destroyed by decay, the
alveolar process by inflammation. Decay of the tooth and inter-
stitial gingivitis are expressions of that natural line of involution
which is foreshadowed from the outset in both by laws of their
development. The laws governing transitory structures natu-
rally place these at the mercy of both under and over stimulation.
From its position, location and functions the mouth is of neces-
sity exposed to invasion of microbes. These tend directly and
indirectly, from infection and through their toxins, to aggravate
the effects of both under and over stimulation. Not only do the
very structure and embryogeny of the teeth and alveolar process
expose them to the too early onset of the processes of removal,
initiated by under and over stimulation, but these last increase
and are increased by the local results of constitutional defects,
like idiocy, and diseases, like tabes dorsalis, paretic dementia,
and allied disorders, as well as the results of injuries to the jaw.

When more work is required of one tooth (as when the
•dental arch is broken by the loss of one or more teeth, and the
others have moved out of their normal position, or when a seam-

148 INTERSTITIAL GINGIVITIS.

stress bites her thread with one or more teeth, or when plates are
attached or come in contact with natural teeth, or when a piece
of bridgework is adjusted) and the roots of one or two teeth
must support and do the work of a greater number, this charac-
ter of adventitious structure predisposes to inflammation about
the root or roots of the teeth.

When due to irregularities of the teeth, or when antagonizing
teeth have been extracted, or in the mouths of idiots, paretic
dements, etc., who do not use their teeth, understimulation also
predisposes to inflammation.

The mass of evidence previously presented demonstrates that
the causes of interstitial gingivitis are divisible into joredisposing
causes (which may be subdivided into local predisposing and con-
stitutional) and exciting causes. The exciting causes are either
constitutional or local, but as a rule are local or have local action.

The predisposing factors of this disease, as already men-
tioned, are : conditions of jaw evolution, transitory nature of cer-
tain structures, degeneracy and conditions of previous irritation
and inflammation.

Moreover, in accordance with a general law of pathology
whereby tissues (for example the lungs in pneumonia once
attacked by toxic agencies or even by the toxins of germs)
acquire a local predisposition to future attacks of disease, the
gums and alveolar process often become thus susceptible to con-
stitutional and local influences.

It is obvious from the data given in the chapter upon "His-
tory " that interstitial gingivitis is as old as man and that it was
observed and discussed by the earliest writers on medicine.
While it is by no means improbable that constitutional factors
assisted in its early progress in man, still the exciting cause of
this disease was tartar. Many skulls from prehistoric periods
exhibit gingivitis upon the teeth exposed to the influence of tar-
tar. This gingivitis extends along the roots nearly or quite to
the apices, resulting in absorption of the alveolar process. Upon
the surface of the teeth where tartar is absent, interstitial gingi-
vitis and absorption rarely occur. The same is true of the
teeth of wild animals at large and confined in zoological gardens.
In them gingivitis from local conditions, other than tartar, very
seldom occurs. The jaws of the skulls of prehistoric periods are

CONCLUSIONS. 149

always broad, measuring '2:1') to 2.50 inches in diameter. Third
molars are always present. The vaults are very low, the alveolar
process short and thick, and the teeth short. As already shown
in the chapter on the "Alveolar Process," the jaws have been
growing smaller until they range in different races from 2.50 to
1.75 inches in diameter. Mixed Celto-Teutonic J races, like the
English-speaking peoples and the Scandinavian peoples, have the
smallest jaws with the most marked deformities as a result.
These changes in jaw forms occur, as has been elsewhere shown,
in harmony- with the law of evolution of the race in face forms.
With these changes in jaw diameter there also occurs an altera-
tion in the antero-posterior diameter. A change in tooth forms
also occurs. Small crowns and long roots replace large broad
crowns and short roots.

These changes necessarily alter the shape and form of the
alveolar processes. Instead of being short and broad, they
become long and thin. The septum between roots is not as wide,
thick or heavy as formerly. The long, thin alveolar process is
more subject to the influence of local irritation and trophic
change than the short, thick one. A long, thin alveolar process
will be more readily absorbed than a short, thick one. This is
demonstrable where the roots of the teeth are situated near the
outer border of the process. Disease of the peridental membrane
and absorption of the 'outer plate extends along the roots, expos-
ing them throughout their entire length. Similar conditions are
noticeable along the palatine roots of the molar teeth in the
upper jaw.

From the length and thinness of the alveolar process result-
ant on the evolution of the jaws, the periosteum on one side
and the peridental membrane on the other hold the structures
together and afford nourishment for the tooth and bone tissue-.
The bloodvessels pass, as elsewhere shown, in a vast plexus from
the periosteum to the peridental membrane through the process.
This plexus deposits and removes calcium salts. Potent for good
under normal conditions, it is equally potent for evil understates
of irritation and disturbed nutrition. Local irritation is greatly

1 Keane, Ethnology.

2 Degeneracy : Its Causes, Signs and Results (Talbot).

Osseous Deformities of the Head, Face, Jaws and Teeth (Talbot).

150 CONCLUSIONS.

assisted by a peculiar structural variation of the gum tissue (R
R, see any figure); accumulation of debris and resultant chemi-
cal decomposition producing inflammation.

Tartar is an. active source of local irritation and inflammation
of the gum margin. This in turn extends through the capilla-
ries to the alveolar process. Calcic deposits are a result and not
a cause.

A predisposing cause for local inflammation is that of approx-
imal tooth decay or cutting away the approximal surfaces for the
purpose of filling this class of cavities. If the teeth be not so
contoured (Bonwill) as to retain them in their proper positions,
absorption of the alveolar process between the roots will take
place, thus bringing the crowns in contact. The result of such
absorption will restrict bone surface for the protection and nour-
ishment of the gum tissue. Undernourished tissues are hence
more liable to irritation and inflammation.

When death of the pulp occurs, the teeth often become loose
without inconvenience to the patient. This results from the for-
mation of gases in the pulp chamber, which suffice to produce
inflammation of the peridental membrane with or without pain.
This occurs, since slight irritation only is needed to produce
absorption of the alveolar process, at the apicial end of the root.
Chronic inflammation of the peridental membrane and the
fibrous tissue of the alveolar process occurs. The teeth finally
become loose. Irritation from movements of the tooth increase
the inflammation through the Haversian canals and further
absorption takes place, until the tooth is exfoliated.

This disease from the onset of gum inflammation may ftroceed
for years without pain. Indeed, not until the formation of
abscess, or until absorption has affected the nerve at the end of
the root does pain occur. Slight soreness may be felt after the
tooth begins to loosen. Absorption of the alveolar process and
exfoliation of the tooth may occur without any pain whatever.

In the chapter upon " Transitory Structures," it has been
shown that the alveolar processes have their structures arranged
to accommodate the teeth. When the teeth are extracted, the
alveolar process becomes entirely absorbed. The periosteum,
peridental membrane and fibrous tissues are entirely lost. The
mucous membrane and gum tissue so contract that none of the

CONCLUSIONS. 151

original structure remains. Absorption of the alveolar process is
very common in advanced age. Even when the teeth remain in
the jaw in old age, whether of man or animal (this is especially
noticeable in old dogs), absorption of the alveolar process con-
tinues. This is due to the fact that the alveolar process, especially
when long and thin, is composed of cancellated hone structure
which is easily acted upon by its abundant blood and Lymph sup-
ply. This produces absorption upon the slightest stimulation or
irritation of nerve fibers. Even such slight factors as heat, brain
overstrain, and want of proper articulation and occlusion and
implantation of the teeth, suffices so to stimulate the nerve fibers
as to produce absorption. There are four varieties of absorption :
osteoclast or lacunar absorption, penetrating canal absorption,
halisteresis, and osteomalaciary absorption. These have already
been beautifully shown in the illustrations. It is. therefore, not
astonishing that the slightest local irritation or tissue nutrition
disturbance from constitutional causes suffices to produce local
tissue change. This unstable condition of structures tends to
prevent successful implantation of teeth.

The question has arisen whether there exists a specific
bacterium, which bears the same relation to the pyorrhoeic
stage that the streptococcus does to streptococcus diphtheria.
This question, raised by Galippe, must, in the Light of careful
research, be regarded as settled in the negative. No special
bacterium has been found which complies with the laws of Koch.
Dogs are Liable to this disease. Galippe had but to infect their
gums with his bacterium to demonstrate its specific pathogenic
activity. Lie has not done this. As the researches (already
cited ) also failed to find a bacterium which could comply with
this test required by the laws of Koch, it must be admitted thai
there is no bacteriologic evidence of a specific bacterium.
Furthermore, the pathologic evidence demonstrates that bacteria
play the very subordinate role in this disease that they do in
ordinary wound infection.

PATHOGENESIS OF INTERSTITIAL GINGIVITIS.

Inflammation of the gums and deeper structures chiefly
results from mechanic and chemic (lactic and uric acid, potas-
sium iodide, mercury, etc. ) causes, bacterial influence being an

152 INTEKSTITIAL GINGIVITIS.

incidental complication. From their action, the blood stream is
increased and dilatation of the capillaries is produced. The
capillaries become crowded with blood corpuscles. These
accumulate along the walls of the blood vessels, to which they
apparently adhere. Accumulations of small, round cells occur
in the submucous connective tissue, the spaces of which are
filled with inflammatory exudate. The papillae become enlarged.
The epithelial layer becomes hyperplastic. As a result, the gum
tissues swell and become intensely crimson. They bleed upon
the slightest touch.

Inflammation may be confined to a single point upon the
side of a tooth. This localization often results from predisposi-
tion due to a local injury, originating in a cavity in the tooth
with sharp, rough edges, from overlapping fillings or from too
frequent and violent use of the toothpick at one point. As a
result, granulation tissue forms, which (according to Sudduth) is
often due to the irritation of lactic acid. 1 In the production of
this, however, the influence of the lactogenic bacteria on particles
of food cannot be excluded.

The peculiar formation of the gum tissue on the inner border
of the gingivus into a pocket or cul-de-sac (RR in Figures) here
described for the first time, is a. fertile source of this irritation
and consequent inflammation, from its collection of resultant
decomposition of foods. This pocket varies, as has been shown,
in size as well as locality. Sometimes it is very large and deep,
or it may be almost, if not entirely, obliterated. Frequently it is
situated near the gum margin, again near the union of the sub-
mucous and peridental membranes. The degenerate epithelium
cell structure (so-called glands of Serres) is also more liable
and more easily irritated than the normal epithelium structure.
As in the similar crypts of the penis, 2 the degeneration and
death of the epithelial cells with which this cavity is lined
produce by their accumulation a source of irritation as well
as culture medium for pathogenic bacteria. Therefore, not
only is the anatomical arrangement of the structures a fruit-
ful source for the accumulation of irritative substances, but

1 1 have made examinations of pockets about the necks of teeth and can cor-
roborate this statement.
2 Medicine, 1898.

CONCLUSIONS. 153

the structures themselves are also well adapted for inflamma-
tory action.

The gum tissue about one or more teeth may be injured by a
badly fitted gold crown, with rough edges. The gold crown may
he too tin- down on the i'oot. Injury may result from ligatures.
rubber dam and hands left about the teeth after operations.
Accumulations of tartar or any local irritation may lead to
inflammation varying with the extent of the deposit. The extent
of the inflammation will depend upon the nature and duration of
the irritating influence. If it he local in action and temporary,
slight gingivitis results. If it he permanent, gingivitis assumes
a chronic type, extends into the fibrous tissue below and becomes
interstitial in character. The extent of this interstitial inflam-
mation depends upon the nature of the irritation. If the irrita-
tion he located upon the side of one tooth, the inflammation will
extend through the fibrous tissue in the direction of the course of
the blood vessels. It may he in line with the peridental mem-
brane. It may he in line with the periosteum, or it may he
in direct line with the alveolar process. Interstitial inflammation
( if one or more teeth be involved) extends not only through the
peridental membrane, hut to the periosteum and alveolar process-
as well, since the capillaries in surrounding structures are in-
volved. The inflammation extends into the alveolar process
through the Haversian canals and the blood vessels of You Ebner
by way of the periosteum and peridental membrane. Irritation
thereon resultant causes absorption of the alveolar process by ( a )
halisteresis, (h) Volkmann's perforating canals, ( <•) lacunar
absorption (osteoclasts). The interstitial inflammation and the
absorption of the alveolar process continues so long as the irrita-
tion remains or until the tooth or teeth are exfoliated. Previous
irritations often produce osteomalacia and trophic changes, and
thus assist greatly the progress of the pathologic phenomena.
Loosening of the tooth or teeth adds a very efficient irritation
which increases the extent of and intensities the inflammation.
Loosening of the teeth is their death knell, no matter what the
original cause for the disease may have been.

The following complications may occur: Endarteritis Oblit-
erans, Absorption of the Alveolar Process, Pyorrhoea Alveolaris,
and finally ( alcie I )eposits.

154 INTERSTITIAL GINGIVITIS.

ENDARTERITIS OBLITERANS.

Endarteritis is an inflammation of the internal coat of an
artery or capillary, generally of chronic type. Its pathogeny is
as follows : In direct contact with the blood streams is the
endothelium (a layer of flattened cells); next is the tunica
intima, composed of elastic fibers arranged longitudinally ; next
comes the middle coat, composed of muscular fibers arranged
transversely. The outer coat consists of longitudinal connective
tissue, which contains the vasa vasorum. In the capillaries, the
intima lies in immediate contact with the surrounding tissues, or
accompanied by a rudimentary adventitia. tn other words, the
walls of the capillaries consist of almost nothing but the intima.
The capillaries have certain contractility; they contract or
dilate without muscular fibers. The veins probably also have a
certain amount of contraction and dilatation from irritability of

Fig. 04. — Endarteritis Obliterans (Kauf.mann).

A, Adventitia. E, Elastic Tissue between Middle Coat and Intima. M, Muscular.
J, Thickened Intima,

the intima. Each coat of the arteries takes on special type of
inflammation. The causes of endarteritis are numerous. Inflam-
mation of the intima of the blood vessels may be due to irritation
from without or within.

When it occurs from without, any local irritation will set up
an inflammation which may extend to the outer coats of the cap-
illaries. This produces a marked increase of blood. The vasa
vasorum becomes swollen, the white blood corpuscles crowd into
the terminal capillaries and migrate into the extra vascular
space. Rapid proliferation of the round-cell elements takes
place. The walls of the vessels become thickened. Owing to
the projecting intervals of the intima, the caliber of the blood
vessels diminishes (Fig. 04).

CONCLUSIONS. 155

Irritation occurring from within, results cither from trophic
changes in the system from direct irritation from toxaemias, or
from both interdependently. Under these circumstances a germ
disease or other toxins may have an affinity for a certain organ,
tissue or part, and produce irritation in the capillaries in a dis-
tinct part of the body, or the capillaries through the entire body
may become involved. Thus, in typhoid fever, the Peyer's
gland in the intestine becomes involved; in scarlet fever, the
skin or kidney ; in malaria, the liver and spleen ; in Bright's
disease, the kidney ; while in mercurial and lead poisoning and
scurvy, the mucous membrane, and especially the gums, become
diseased. In many of these conditions, however, before the
tissue already irritated becomes involved, the nervous system has
become affected. The nervous system may already have become
■affected from other causes. Thus, locomotor ataxia, traumatic
injuries to the spine, paretic dementia, cerebral paralysis, neu-
roticism and degeneracy, and last, hut not least, stomach neuras-
thenia. The poison in the blood, together with the diseased
peripheral nerves, produce irritation and inflammation of the
inner coat of the capillaries. If this irritation does not disap-
pear soon after its inception, the inflammation tends to affect the
other coats of the blood vessels. ruder certain conditions,
endarteritis may, however, never involve the other coats of the
vessels. When irritation of the inner coat of the capillaries
takes place, proliferation of the endothelium occurs. This
inflammatory growth tends to obstruct the lumen of the vessel.
The media may likewise become thickened by an increased con-
nective tissue. The capillaries become obstructed, and finally
obliterated. This finally impedes the circulation. Fig. 65
shows such a condition in the scurvy case, elsewhere illustrated.

Irritation may he of less intensity hut greater duration, as in
case of syphilis, tuberculosis, scurvy, mercurialism, plumbism
( lead poisoning), etc., and the results are then slowly effected.
Proliferation of sub -endothelial connective tissue gradually
increases until it reaches its limit (endarteritis obliterans). This
influence of the proliferation is exerted in addition to that of the
round-cell infiltration about the structure.

The recent studies of Hektoen ' on meningeal tuberculosis

1 American System of the Practice of Medicine, page 119.

156

I NTERST I T I A L GINGIVITIS.

demonstrate that tubercle bacilli may penetrate the unbroken
endothelial layers of the vessel and stimulate marked proliferation
of the sub-endothelial connective tissue. An internal irritant,
such as may be produced in the course of any infectious disease
or from suboxidation, probably acts upon the endothelium of the
walls of the smaller blood vessels in such a way as to permit the
escape through the walls first of serum, then of leucocytes, the

Fig. 6o.— Cr
C, Cementum. D

X ISO. D. D. obj. Zeiss.
Section of Peridental Membrane, Showing Endarteritis
Obliterans. Scurvy in Man.

Dentine. I, Peridental Membrane.
EO, Endarteritis Obliterans.

IT, Nerve

latter infecting and surrounding the vessels. The effect of the
chronic endarteritis is to check the blood supply to the gum
tissue. Mercury, lead and other poisons circulating through the
blood are forced to remain, hence discoloration of tissue along the
gum margin. Interstitial gingivitis, resulting in a slow disturb-

CONCLUSIONS. 157

ance of nutrition, produces overgrowth of connective tissue. In
all cases of chronic interstitial gingivitis, as shown in the illus-
tration, arc the blood vessels thus involved.

Among the predisposing influences which cause this disease
are syphilis, tuberculosis, mercurialism, plumbism, brass poison-
ing, lithaemia, nephritis, gout, rheumatism, alcoholism, scurvy,
nervous diseases, pregnancy and old age. Under certain con-
ditions of the system any and all diseases which tend to lower the
vitality, producing anaemia, will assist in producing this disease.
The direct cause may be resultant overstrain of the blood vessels.

Owing to obliteration of the arteriols in the alveolar process
stasis of blood must follow. The detritus from the alveolar pro-
cess, therefore, must remain in the tissue and collect upon the
roots of the teeth.

ABSORPTION OF THE ALVEOLAR PROCESS.

Absorption of the alveolar process is the result of irritation,
resultant malnutrition, and subsequent inflammation. The osteo-
blasts and osteoclasts are ever present to build up and tear down
bone structure on the slightest provocation. Hypertrophy
(building up of bone tissue) is the result of intermittent pressure,
and atrophy, or absorption of bone, is due to constant irritation
and pressure. As has been elsewhere shown, from its transitory
nature the alveolar process is unusually susceptible to these influ-
ences. The causes of absorption are loss of teeth by extraction,
undue pressure upon one or more teeth from improper articulation
(Bonwill), wedging and irregularity correction, heat under arti-
ficial dentures, and interstitial gingivitis of local and constitutional
origin.

According to Kaufmann, lacunar absorption is the most
common type. This may be true in morbid anatomy of bone
tissue generally, but it is not true of absorption of the alveolar
process. On an examination of hundreds of slides prepared
from canine and human jaws (of which characteristic types arc
illustrated), by far the most common form of absorption was
found to be halisteresis. Perforating canal absorption, which
Kaufmann has "occasionally met with," is certainly very com-
mon, while lacunar absorption holds third position. This order
of absorption is accounted for by the fact that where structures

158 INTERSTITIAL GINGIVITIS.

are transitory, halisteresis, as quickest method, follows by the law
of the survival of the fittest. For the same reason perforating
canal absorption should stand second. • The blood vessels of Von
Ebner being most numerous, although considered smaller, they
would naturally be the second tissue involved. As in interstitial
gingivitis, absorption of the alveolar process is invariably due to
inflammation, halisteresis apparently starts at the larger Haver-
sian canals from which this form of absorption invariably
originates.

Interstitial gingivitis extends to the alveolar process through
the periosteum as well as the peridental membrane (not, as den-
tists usually believe, by way of the peridental membrane alone).
This is demonstrated by the illustrations. The entire alveolar
process thus becomes involved. The products of inflammation
extend through the Haversian canals (a path obviously evident
in pathologic illustrations), setting in action the three forms of
absorption as elsewhere illustrated.

Halisteresis Ossium ( doXo? of salt, ere/tims deprivation ) or
decalcification, is that process of absorption wherein solution of
the lime salts first takes place, while the cartilage or matrix
remains for the time undisturbed.

Solution of the lime salts begins at the periphery of the
Haversian canal and advances toward the center of the tra-
becule. This absorption follows, as a rule, the bone layers. Bone
centers are, therefore, usually the last to be absorbed. Fre-
quently decalcification becomes complete; nothing remaining but
the organic matrix or cartilage. Finally, this is also entirely
destroyed. As the osteoblasts occur in the matrix or cartilage,
it is not difficult to understand that absorption may extend far,
yet restoration of the alveolar process may occur. After destruc-
tion of the matrix such a restoration is impossible. New fibrous
tissue may be partly restored, but it is doubtful if the alveolar
process can be.

Both Ziegler 1 and Kaufmann 2 divide osteomalacia into senile
and juvenile. The latter occurs most frequently during jjreg-
nancy. In senile absorption, after a certain period, the entire
skeleton is affected. The condition begins most frequently in

1 Special Pathological Anatomy, page 151.
2 Pathologische Anatomie.

CONCLUSIONS. 159

the "vertebrae and thorax; Inter extending to the extremities."
In pregnancy "the pelvic bones are first involved, the process
then extends to the other bones." It is singular that the alveolar
process should have been so much neglected by pathologists,
since, in both states, the alveolar process becomes involved long
before the bones of the body.

This is due to three reasons: first, to trophic changes; sec-
ond, to the alveolar process being a transitory structure; and
third, to improper care of the gums at these periods.

Osteomalacia occurs in the alveolar process much earlier than
at the so-called "senile" period. It is found at twenty, or even
earlier. At any period beyond that year, it occurs probably from
the prematurely senile states of which precocity is a type. The
lost tissue is regained often after confinement in the " preg-
nancy" type, but is never regained in the senile.

The causes which produce morbid decalcification are not thor-
oughly determined. Some believe it to be due to lactic acid in
the system, others attribute it to an increased amount of carbonic
acid in the blood. Eisenhart believes it to he due to a want of
alkalinity of the blood, while Von Reehlinghausen charges it
to a local irritation of the vascular mechanism of the bones. It
would seem, from examinations already cited, that, so far as the
alveolar process is concerned, local irritation from biochemic
changes in the blood, as suggested by Von Rechlinghausen, i>
the chief cause. Premature absorption of the alveolar process
accompanies the movement of the teeth in their correction or in
rapid wedging. Frequently the alveolar process is never fully
restored, thus producing a predisposing factor for future disease.

Premature absorption, or osteomalacia of the alveolar process,
is easily recognized. A shrinking of the gums and alveolar
process exposing the necks of the teeth is very conspicuous.
Frequently the gums and mucous membrane covering the alveo-
lar process is quite red (this is very noticeable in dogs), and a
thinning of the alveolar process over and between the roots of
the teeth. The process of one tooth only may become involved :
again the process over two. or the whole jaw. and again both jaws
become affected.

When osteomalacia occurs, either of pregnancy or senile
type, although the tissues he seemingly restored to health, struc-

160

I XTHKSTITI A L GINGIVITIS.

tural change has taken place to such an extent that it ever
remains a predisposing factor to interstitial gingivitis.

In Fig. 36 may be seen the blood vessels of Von Ebner.
These blood vessels are also to be observed in Fig. 55. They
are very common in the alveolar process and, according to Volk-
mann, are the source of the perforating canals which bear his
name.

X ?>o. !i-ineli obj. No. Oe.

Cross Section or Tooth, Alveolar Process and Peridental Memrrane,
Showing Lacunar Absorption. Man.

Fig. 66,

C, Oenientuin. D, Dentine

I, Peridental Membrane.
0, Lacunar Absorption.

J, Alveolar Process.

These canals run in all directions. After absorption has gone
on to form medullary spaces, these canals penetrate through the
trabecule from one space to the other (Fig. 38). The position of
this type of absorption in the order of frequency conies from the
fact that, in this disease, absorption is almost entirely due to

CONCLUSIONS

inflammation ; hence the blood vessels are the first to become
involved. Those entering the Haversian canals, being the larger,
are first affected, and hence halisteresis naturally precedes.

When irritation takes place in a nerve or part of hone which
is about to he absorbed, multinuclear cells arise at the border in
the periosteum and peridental membrane. They attach them-
selves to the surface of the bony trabecular. According to Sud-
duth, "the absorber and the absorbed must be in touch with each

ULit:

x 300. No. 2, projection ocular. D. D. obj. Zeiss.
Fig. »>7. — Section of Peridental Membrane, Showing Lacunar Absorption in Dog.
.1, Alveolar Process. O, Lacunar Absorption. I 1 , Inflamed Peridental Membrane.

other." Kolliker has named these cells "Osteoclasts," which
term has come into general use. Very soon after these cells
make their appearance, cavities are seen in the hone tissue.
These cavities are called Howship's lacuna?. Lacunar absorp-
tion, as elsewhere shown, takes place as a result of irritation and
overstimulation. Fii>\ 66 shows a cross section of the end of one

162 INTERSTITIAL GINGIVITIS.

of the buccal roots of Fig. 68. As will be observed, this tootli
was held in place by two buccal roots. As much resistance was
required of these two roots as was formerly required of three.
Irritation due to excessive force in mastication was causing
absorption. Round-cell inflammation is not present in the peri-
dental membrane. The irritation may be continued until inflam-
mation sets in and until the bone is entirely absorbed, as noticed
in Fig. 67. Small round-cell inflammation is quite noticeable in
the surrounding tissue.

Sometimes these lacuna? may be -seen extending along the
entire length of bone. As many as thirty-seven may be counted
in some fields (Fig. 37). Lacunar absorption frequently so
extends through the Haversian canals as to cut off pieces of the
alveolar process. A casual glance at Fig. 66 demonstrates this.
This figure could be multiplied many times from other slides.
These frequently come away with the peridental membrane when
the tooth is extracted. This is often noticed in removing loose
teeth due to interstitial gingivitis. By passing the finger over
the surface of the root, the rough pieces of bone may be easily
felt,

Aside from the forms of absorption already noted, absorption
of the alveolar process is often seen, the result of neuropathic
lesions. Paretic dementia, diseases of the spinal cord, low forms of
inflammation, general debility and traumatism, together with
unhygienic conditions of the mouth, are fruitful sources of inter-
stitial gingivitis and absorption of the alveolar process. Absorp-
tion of the alveolar process takes place also in diathetic diseases
in which the nervous system has been involved (syphilis, scurvy,
lithsemia, etc. ).

PYORRHOEA ALVEOLARTS FROM INTERSTITIAL GINGIVITIS.

Recovery from interstitial gingivitis and return to normal
conditions without change in structure is called restoration.
Should the damage be extensive, and accumulations of cell and
liquid exudate so press upon the tissues as to extinguish their
vitality, ordinary restoration is impossible. This is also true
when the inflammation is more decided and persistent. This
inflammation may extend throughout the tissue. Absorption of
the alveolar process may take place, and exfoliation of the teeth

CONCLUSIONS. 163

result without pus infection. The tissues may be in a favorable
condition for infection, yet the mouth and blood vessels be free
from pus germs. This is not uncommon. The tissues are often
invaded, however, by micro-organisms, resulting in suppuration.
Interstitial gingivitis, with pus infection in and about the alveolar
process, resembles suppuration elsewhere in the body. It results
either in an abscess or ulceration. An abscess is a collection of
pus within the tissues. Ulceration is a collection of jms upon
the surface of the tissues. Both of these marked conditions.
being dependent upon inflammation, are associated with intersti-
tial gingivitis.

Suppuration (due to pyogenic cocci) is the usual termination
of infective inflammation. Healthy gum tissue is intolerant of
bacteria, and will resist the invasion of micro-organism. When
inflammation takes place, the diseased part is unable to resist
them. Lowered vitality of tissue is a fruitful source of infection
and suppuration. Since, as Miller 1 has shown, pus germs are
found in almost every mouth, infection is a very probable outcome
of gingivitis.

The organism most frequently producing pus are the staphy-
lococcus pyogenes aureus, and albus. These have a tendency to
accumulate in groups. When they collect at a given point in the
tissue, suppuration results. The streptococci ( occasionally pres-
ent in the mouth) do not as a rule produce local suppuration, but
spread through the tissue by way of the Lymphatics and blood
vessels, and eventually give rise to abscess. The delicate reticu-
lum of the blood vessels found in the Haversian canals is a
convenient lodging place for swarms of bacteria, owing to the
slowness of the blood current and the tortuous course of the
blood channels. When 2 the circulation has been impeded or
arrested by an extravasation of blood or congestion of a part, the
conditions are favorable for intravascular infection if organism
happen to be circulating in the blood at the time. As we have
-ecu, micro-organisms may from time to time be found in the cir-
culation, particularly in individuals of feeble constitution. The
anatomic nature of the part will therefore determine suppuration
in certain localities.

Micro-Organisms of the Human Mouth
American Text-Book of Surgery.

164 INTERSTITIAL GINGIVITIS.

In whatever part or tissue the change may occur, the process
is the same. The original structures disintegrate. Their place
is taken by a closely packed crowd of migrated leucocytes.
Should the cause continue to act, the process culminates in the
formation of pus. The migrated cells cut off from proper
nutrition by pressure are exposed to the injurious action of
micro-organism. The central cells of the group degenerate from
want of nutrition or die from direct action of the irritation. The
intercellular substance softens, and the liquid exudate from the
surrounding parts mingles with the broken-down tissue to form
an abscess.

As I have shown, foci of infection and intense inflammation,
to the point of degeneration and liquefaction, occur in most
every locality within the peridental membrane, periosteum and
alveolar process. These abscesses are just as likely to point
upon the surface of the gum as on the inner surface next to the
root of the tooth. When abscesses form in and about the
alveolar process, with fistulas opening outside of the inner
alveolar wall, the disease cannot be entitled pyorrhoea alveolaris,
since, as elsewhere shown, strict definition of this title implies
pus flowing from the alveolus.

Abscesses which discharge their contents into the space
between the alveolar wall and the root of the tooth, and ulcer-
ation of the peridental membrane only, could literally be con-
sidered under the head of pyorrhoea alveolaris.

Abscesses in and about the alveolar process (other than those
due to dead pulps) are very common. This is due first to the
unstable condition of the structures, and second to the ready
access of pus germs through the inflamed gums and peridental
membrane. Those most susceptible to infection are patients who
are anaemic and below par in vitality, and whose gums have
become inflamed either from local or constitutional causes.
Especially is this the case in those who have osteomalacia
where the gums have receded quite a distance from the necks
of the teeth. Pus germs collect at the necks of the teeth, infect
the raw inflamed surfaces of the epithelial layer, and entering
the circulation are carried into the deeper structures. Intense
inflammation results. Abscesses form, discharging their con-
tents upon the surface. Pus germs also enter the deeper struc-
tures through exposed pulps.

CONCLUSIONS. L65

Two cases of interest in this connection occurred recently in
practice. An active business man, fifty-five years of age, pre-
sented himself with an abscess over the buccal roots of the left
superior second molar. There were no dead pulps in any of the
teeth upon that side of the jaw. Absorption <>t' the alveolar
process and contraction of the gums had occurred around all the
teeth. He had been overworked and was nervously exhausted.
Five years ago cataracts were removed from both eyes. He is
exceedingly sensitive to pain. Examination of blood revealed
slight anaemia. On examination of urine, other than a specific
gravity of 1028, it was found normal. The abscess was lanced
and cavity cleansed. It healed within a week. Subsequently
he returned with another abscess over the root of the right
superior central incisor. Live pulps were in all the teeth upon
this side as far as the second molar. Infection, therefore, must
have occurred through the gum and peridental membrane.

The teeth of a lady forty-six years of age were being put in
order; after filling a cavity, May 14, 1899, she called attention
to a space between the second and third superior right molars,
and stated food lodged at that point, causing pain and bleeding.
The space was cleansed with an excavator and the cavity
syringed with warm water and then explored. Absorption of
the gums and alveolar process had extended one-half the length
of the buccal root. Applications of iodin were made to reduce
the inflammation. The patient was dismissed with an appoint-
ment for May 17. She returned at the appointed time with an
abscess over the palatine root as large as the thumb. The lady
had had acute pain from the time she left the office until her
return. The parts had been infected with pus germs through
the peridental membrane. The pus was collected in a tin tea
spoon, from which cultures were obtained and glass slabs
smeared for microscopic examination. The pus was examined
by George T. Carpenter for calcic deposits ; the usual aseptic
precautions having been taken.

Microscopic examination revealed the usual pus germs.
Chemical analysis for calcic deposits in the pus was made as
follows: The pus was placed in a test tube with hydrochloric
acid (diluted with four times its bulk in water). The phosphate
is dissolved. It is then diluted with water, boiled, and when

160 INTERSTITIAL GINGIVITIS.

cold excess of solution of ammonia added. The lime salts are
then re-precipitated as an amorphous powder.

Many dentists, ignoring the laws of pathology, insist that
intense inflammation in remote parts of the alveolar process is
not due to invasion by micro-organisms of an inflamed tissue,
but is the result of gouty deposits. The utter lack of foun-
dation for this theory must be apparent on the slightest study
of pathology.

Ulceration is always located upon the surface of a tissue.
When ulceration occurs from contact irritation of the gum margin
or by mechanical or chemical means, congestion and oedema
result, thickening of the epithelial layer and increased growth of
cells. The sub-epithelial tissue becomes inflamed. The process
is not unlike that of the formation of an abscess, since the
infected tissue resembles part of an abscess wall. In slowness of
progress only does ulceration differ from acute inflammation.

Such is the condition of the peridental membrane. When
simple gingivitis becomes chronic, the inflammation extends to
the surface of the peridental membrane. This is situated at the
Lower extremity of a cul-de-sac, formed by the gum on the one
hand and the tooth on the other. This cavity is filled with
foreign material in which decomposition continually occurs.
The tissues are thereby constantly irritated. Necrosis occurs at
the surface. In the deeper tissues that' have become inflamed
pus cells also are found. These not only arise from the normal
blood vessels in the vicinity, hut also from the granulation tissue.
The causes of peridental membrane ulceration are disturbances of
nutrition, endarteritis obliterans (a disease of the blood vessels
due to constitutional diseases, such as syphilis, scurvy, tubercu-
losis, uric acid and other blood poisons) and starvation of tissue,
feeble circulation (as in anaemia) and inflammation. If the
ulcerated surface be examined under the microscope, a general
thickening of the tissues will be seen. In the papillary layer
deposits of blood pigment (Fig. 52)' occur. The surface is
covered with granulation tissue. The tissue may, in part,
resemble the type of healthy granulation. It is composed of
round cells closely packed together and supplied with rich capil-
lary network. Coagulation necrosis from breaking down of
granulation tissue may be present.

CONCLUSIONS. 167

CONSTITUTIONAL EFFECTS OF PYORRHCEA ALVEOLARIS.

The influence of the stage of interstitial gingivitis known as
pyorrhoea alveolaris on the system has been discussed by John
Fitzgerald. 1 He points out that pyorrhoea alveolaris may act in
three different ways in the causation of systemic disease. The
pus, with its multitude of putrefactive organisms and decayed
food remnants from the pus pockets, may be swallowed and either
act locally upon the stomach wall or set up fermentation of the
stomach contents. The toxins generated in the month may be
absorbed by the mucous membrane of the mouth or stomach and
thus pass into the general circulation. The local conditions of
the mouth may favor the growth of pathogenic organisms, and
thus render the patient more liable to certain infectious disorders,
noticeably influenza. The power of pyorrhoea alveolaris to pro-
duce aggravation of existing gastric trouble reaches its maximum
in cases where there is retention of food residues. This happens
when the muscular walls of the stomach are in a state of atony
and also when there is some pyloric obstruction which prevents
the organ emptying itself. In both these conditions stomach
dilatation is eventually produced, with the result that the stomach
is never completely emptied. -The first condition is a very fre-
quent concomitant of neurasthenia and allied states. It is easy
to see how pyorrhoea can at once be predisposed to by neuras-
thenic states and at the same time increase the neurasthenia by
causing gastric trouble through its interference with gastrointes-
tinal digestion under the conditions mentioned.

Herschell 2 is of opinion that many of the chronic indigestions
are due to continual absorption of pus into the system from a
pyorrhoea alveolaris. In these cases he remarks there should be
other evidences of the absorption of toxins, such as pigment spots,
urticaria, etc. Fitzgerald points out that the bacterium coli com-
mune is a constant inhabitant of the oral cavity, and, as a rule,
seemingly harmless. Under the influences of a culture medium
such as would be furnished by a pyorrhoea or an inflammatory
state of the gum, this bacterium might, as elsewhere in the
mucous membrane, acquire sufficient virulence to produce serious
disturbances of the system, such as colitis, dysentery and cholera
nostras.

Clinical Journal, March (i, 1899. - Indigestion, 189.").

1(58

INTERSTITIAL GINGIVITIS.

CALCIC DEPOSITS.

There are many instances in which interstitial gingivitis takes
place, with absorption of the alveolar process and exfoliation of
the teeth, without calcic deposits. In such cases the blood is
charged with only sufficient lime salts for the nourishment of the
body. The waste products are carried off with the excreta. In
absorption of the alveolar ju-ocess, inflammation does not seem to
extend to the capillaries, the result of which is, this waste mate-
rial is curried into the circulation. In this way, calcic material

Fig. CS.

does not collect in the fluids and upon the teeth. In those cases
in which pus is not present (there being a lessened amount of
carbonic acid) calcic deposits rarely take place. The percentage
of teeth so found, however, is not so large as those with deposits.
Examination, by a magnifying glass, of a recently extracted
tooth (whose root is covered with serumal deposits) shows the
lime deposited in a manner resembling that of stalactite forma-
tion. The deposits often stand out distinctly independent of each
other ( Fig. 68). This condition is due to deposits from the blood,
resultant on biochemic changes in the inflamed tissues. Blood

CONCLUSIONS. 169

stasis occurs in the gum tissue, fibrous tissue of the periosteum,
peridental membrane and alveolar process, through which last
much of the blood circulates. This stasis may be consequenl
upon conditions varying from simple inflammation to disease of
the endothelium, producing endarteritis obliterans.

The blood has become surcharged in all constitutional dis-
eases, but more especially in kidney lesions. Deposits occur in
the fluids and upon the roots of the teeth. Frequently the
deposit is found only on one side or only at one particular spot
on the side of the root ; again at the apex, when the pulp is
destroyed. It may encircle the root. The inflammatory process
may therefore be circumscribed as to area or the whole tissue
may be involved. The deposit is circumscribed in the area of
inflammation. The calcareous matter absorbed from the alveolar
process in the immediate vicinity of the root is not improbably
soon deposited upon the root or roots because of the impeded cir-
culation. 1 "Ossification, as has been well remarked, is an active
development in which the tissues are abundantly supplied with
blood. There is a rapid cell proliferation, and the calcareous
matter forms an intimate and permanent union with the tissues.
Calcification, on the other hand, is passive, and indicates an
impaired vitality. Calcification begins as a rule in the intersti-
tial tissue. In regard to the origin of the calcareous salts, it is
generally believed that they come more or less immediately from
the blood, although Rokitansky supposes that they were formed
by a metamorphosis of the tissues involved."

Calcification is due to two varieties of causes: general and
local. The former are dependent upon changes in the blood or
its circulation, due, for example, to disease or senile change. In
composition the blood may he so altered as to contain an abnormal
amount of calcareous matter. This effect is most commonly pro-
duced by absorption of lime salts from osseous tissues which are
the seat of extensive caries, osseous cancer, osteosarcoma or osteo-
malacia. The calcareous matter thus taken up is conveyed to
other and often remote parts and there deposited, constituting the
" metastatic calcification " of Virchow. Kiittner, of St. Peters-
burg, has observed a rapid calcification of nearly all of the small
arteries as a result of caries involving the dorsal and lumbar

1 Wood's Handbook of Medical Sciences, Vol. I, page 74:!.

170 INTERSTITIAL GINGIVITIS.

vertebrae in a nineteen-year-old boy. Virchow has observed a
case in which, as a result of bone cancer (affecting nearly all of
the larger bones, particularly the borders of the vertebra and the
skull), the calix and pelvis of the kidneys, the lungs, parenchyma,
and the stomach mucous membrane were calcified.

Circulation of the blood may be retarded and thus favor pre-
cipitation of calcareous matter normally held in solution. To this
is chiefly due the frequency of calcareous degeneration from
general loss of vitality.

Calcification rarely, if ever, depends upon general causes
alone. There is, as a rule, a local influence. Very often this is
due to preexisting chronic inflammation. Old accumulations of
pus and exudates are exceedingly prone to calcification. The
deposit frequently occurs also in fibrous walls surrounding the
accumulation. A mere loss of function predisposes to calcification.
Such is the case in and about the tissue of the alveolar process.
The decalcified material from the alveolar process collects in the
soft tissues as well as upon the roots. In his paper George T.
Carpenter ' asks the question : Can a tissue be absorbed and still
remain as debris in the pocket? Such is the condition found,
and this can be easily proven. Take the contents of a pocket
and dissolve it in hydrochloric acid, add three times its bulk of
water, to this add ammonia, which will precipitate the phosphate
and the calcium. The same results may be obtained by rinsing
a freshly extracted tooth of a pyorrhoea case in cold water.
With a stiff brush remove the accumulation and place it in a
test tube, add hydrochloric acid and more water if necessary.
To this add a solution of ammonia and the lime salts are precipi-
tated.

Roots of teeth that have become entirely denuded of peri-
dental membrane and bathed in pus accumulate large quantities
of calcic deposits direct from the absorption of the alveolar
process.

Difference of opinion exists as to the nature of the process
immediately involved in precipitation of lime salts. The simplest
and seemingly most logical explanation is that the process is
similar to that involved in the formation of stalactites. A certain

1 Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhea
Alveolaris,

CONCLUSIONS. 171

amount of calcareous matter is a normal constituent of the blood.
Herein it is held in solution by carbonic acid, always present in
sufficient quantity for this purpose. When the circulation is
impeded the free carbonic acid (because of its great diffusibility)
is readily absorbed by the tissues or goes to form new compounds,
necessitating a precipitation of the calcareous matter. Calcareous
matter may be deposited in either a fibrous or fluid matrix. It
shows a preference for newly formed fibrous tissue, particularly
when this is associated with old tissue undergoing fatty degenera-
tion and absorption. In a fibrous matrix the infiltration usually
begins in the intercellular substance, but may involve the cellular
elements at a later period. In a fluid matrix (like pus) the
granules are frequently deposited primarily within the cells. The
process may advance slowly or rapidly. When local causes exert
the chief influence it is more limited in area of invasion than
when there is a general factor in its production, as in the meta-
static forms.

CHAPTER XVI.

TREATMENT.

The .clinical history of interstitial gingivitis is essentially that
of any other disease of the mucous membranes. The disorder
responds quickly to treatment at its outset. Later, its complica-
tions and the extent of structure involved render treatment very
inemaeious, and always insure loss of the tooth. As the general
surgeon's duty is to save life, if need be, at the expense of limb
or organ, but to save these last if possible, so the dental surgeon's
duty is to remove the teeth, if need be, for the benefit of the
general health, but to save them, when possible, for the same
reason. The patient, therefore, should be told frankly at the
outset of interstitial gingivitis, that it is a condition requiring
time for its treatment, and should not be given that prognosis
too frequently made of quick cure. To such a prognosis many
a case of constitutional disorder is due. The dentist is a practi-
tioner of a surgical specialty, not a mere tooth-puller. The sur-
gical side of dentistry has received too much attention, however;
the medical or prophylactic too little. Patients are beginning to
pay more attention to the prophylaxis of the teeth and jaws, and
need but little encouragement and instruction to see the absolute
necessity of early prophylaxis and treatment of interstitial gin-
givitis. The trend in general medicine is to prophylaxis, and
this has undoubtedly so impressed patients as to open the way
for dental prophylactic suggestions. Viewing the question from
the narrowest standpoint of remuneration, the dentist could not
fail to profit by instructions to his patients on prophylaxis. He
certainly tails in his duty as the member of a learned profession
by not doing this. Furthermore, with the known necessity for
prophylaxis, it is an open question whether the failure to inform
the patient of the clangers of the incipient disease could not be
successfully pleaded as a basis for a malpractice suit.

From the etiology of this disease, the treatment would appear
simple and easy.

TREATMENT. 173

Early diagnosis is not difficult, since the simple inflammation
of the gums is easily recognized by the patient. Bleeding when
the toothbrush or toothpick is used can never be mistaken.
The dentist with his accomplished eye can readily detect the
slightest change in color or puffiness around the necks of the
teeth or of the festoons between the teeth. Redness, puffiness
and bleeding are pathognomonic of this disease in its incip-
ience.

Few dentists have, however, given this stage of the disease
any thought, albeit they have filled the teeth of their patients
from year to year. 1 have in mind three patients with loose
teeth and inflammation extending throughout the peridental
membrane and alveolar process, who had been under an old
practitioner now retired from practice. The patients had never
had the gums treated or even their teeth cleaned. This is not
an uncommon occurrence. The excuse usually made by the
dentist is that he cannot get paid for his time. Gingivitis is
a disease which the dentist is as much bound to treat and cure
as any disease of the month and teeth. It is a part of his
specialty which should not be ignored. It is claimed that the
dental profession is overcrowded. Were this disease treated
until the gums were placed in a healthy condition, there would
he practice enough for as many more dentists as there are today.
The busy dentist of today could attend only to one-half the
patients whom he now serves.

The treatment, then, should be prophylactic in its nature,
preventive rather than corrective. The disease and treatment
is not unlike an inverted pyramid : the farther from the apex or
beginning, the more difficult and hopeless the task becomes.
Since the teeth have nothing directly to do with this disease,
they should be ignored. In the early stages, the gums should
receive proper attention. These, like other parts and organs of
the body, must be exercised to be kept healthy. The gums
should be properly massaged, just as the liver, kidneys or skin
are when they are not doing proper work. This can he accom-
plished by properly made brushes. The ordinary toothbrush is
not adapted to the work under discussion. It will brush the
teeth hut not reach the gums. What is needed is a massage
hrush that will miss the teeth to a certain extent, but will reach

174 INTERSTITIAL GINGIVITIS.

the gums and contract them tight around the teeth, thus pre-
venting the accumulation of foreign substances. The patient
should be instructed with this single idea in view, " that the
gum margin is to be exercised and stimulated and not the teeth,
which must be ignored." A brush, properly made for gum
massage (Fig. (39), will do sufficient work upon the teeth with
the aid of the floss silk and toothpick. It should haVe printed
upon the handle, in large letters, " gum massage brush." The
handle should be bent a little more than the " prophylactic," so
that the end containing the bristles can he brought in contact
with the gum, posterior to the central incisors, upper and lower,
and around the third molar teeth. There should be a tuft of
bristles at the point with a space for the teeth. The tuft should
he longer than those on the body of the brush. This tuft will

reach the gums at all points inside of the mouth and around
the molars. The bristles on the body must have spaces between
them, so that when the upward and downward movement is
given, the bristles will go between the teeth and reach the gum
festoons. The bristles must be medium and hard. The quality
of bristles must depend, however, upon the condition of the
gums. If they be soft and spongy, the medium may be used.
If the processes are heavy and thick, the gums swollen and
engorged with blood, hard bristles must be used, Soft bristles
(although sometimes recommended) should never be used.

The antique theory that vigorous stimulation is injurious is
too much accepted. Barrett, 1 for example, says, "massage of the
gums with the ball of the finger and by the frequent use of a
rather soft brush should be resorted to." Beodecker ' remarks
that too frequent application of the toothbrush is sufficient to

1 Dental Cosmos, 1883, page ">•'!:.'.

2 Anatomy ami Pathology of the Teeth, page :;ii.">.

TREATMENT. 175

produce papillary hyperplasia. Tomes 1 says, " in my own expe-
rience I have found that frequent and vigorous rubbing of the
gums with the finger, shampooing them in fact, has often been
productive of great advantage, the patient of course being cau-
tioned not to rub the actual edge; but even on this point there
is difference of opinion, for in a recent paper on the subject, rest
and the avoidance of all friction is advocated." Dr. Meyer L.
Rhein 2 in introducing the "Prophylactic Toothbrush" to the
profession, says, in his article on "Oral Hygiene," each brush
conies inclosed in an envelope, upon which are printed directions
for the intelligent use thereof, and the following caution : "Never
pass the brush across the teeth, as this movement destroys the
delicate membrane which attaches the gum to the teeth, causing
recession of the gum, and ultimate loosening and loss of the
teeth." Citations of this could he multiplied, showing the gen-
eral impression is that the gums should not he stimulated to any
great extent; that the finger, a soft cloth, or a very soft tooth-
brush alone should he employed. The use of the finger is a
superstition which is handed down from generation to generation
without the slightest critical analysis. If the advocate of this
use would try the experiment, he would see how impossible it
would he to bring it in contact with all the tissues of the mouth
that are involved in this disease; were it possible, the lingers,
cloth and soft toothbrush would not accomplish the desired
result.

No brush should he used whose bristles are softer than the
medium ; very often these, used once or twice and dipped into
water or mouth washes, become so soft as to he wholly unfit for
use. It is always a good plan to have two brushes to be used on
alternate days. In this way one can dry while the other is being
used. The general opinion has been that friction upon the gums
was detrimental on account of the resultant tendency to absorp-
tion of the gums. While this may exceptionally he true, it is
not true of a majority. Should milk, arsenic, iron, strychnine or
quinine he entirely abolished as remedies because occasionally a
person presents untoward effects? If the alveolar process he
very thin over the roots of the teeth, especially the cuspids, the

1 Dental Surgery, page, 704.

-New England Journal of Dentistry, October, 1884.

176 INTERSTITIAL GINGIVITIS.

patient must be instructed so to use the brush as not to over-
stimulate these particular parts. In such cases the inner alveolar
process and gum tissue may be stimulated with impunity and
with the hardest brush. Again, if the chronic interstitial gingi-
vitis be of long standing, or even if chronic gingivitis has
been present for some time, stimulation of the brush will
cause the gums and mucous membrane to recede until hard,
sound, healthy structure has been secured. Then absorption
will cease. In most cases absorption and contraction of the gum
tissue will take place to a more or less marked degree. If
absorption of the alveolar process has taken place and the gums
are puffy, red and swollen, a disease exists to be cured, regardless
of consequences. The alveolar process and gums will never
return to their original jjosition, but it is a decided advantage to
have a healthy mouth, even if the alveolar process and gums
have slightly receded.

I have used medium and stiff brushes in my practice for the
last fifteen years and have failed to see any ill results. For the
past four years I have made constant experiments, with the view
of securing the proper shape and stiffness of the bristles and have
obtained uniform results in gum treatment.

Proper employment of the " gum massage brush " requires skill.
Every dentist should train his patient in the method of using the
brush. The gingival borders should not only be stimulated, but
the bristles should be so passed in between the gum margin and
the tooth as to remove the debris and exfoliated epithelial scales
which have accumulated therein. These are often the cause of
the irritation. Unless this be done the gum or epithelial tissue
cannot perform its functions or be restored to health. Stimulat-
ing astringents and germicidal mouth washes should be employed
whenever the gums are massaged. The massage should be done
three times a day. The patient should be under the care of the
dentist at least twice or thrice a week, so that he may direct the
treatment, If the teeth are irregular, care and patience are
required to reach the festoons between the teeth. After the gums
are in perfect health, the patient should visit his dentist at least
four times a year for further instruction. If on inspection the
gums be found diseased at any point, the dentist can direct the
attention of the patient to the particular locality and the disease

TREATMENT. 177

be eradicated. By this method and this alone can the gums be
kept in a healthy condition. Each patient must be given specific
directions as to the treatment of his or her case.

If the gums have become swollen and engorged with blood
a different method must be employed. Here the absolute law of
medicine obtains — "remove the cause," no matter whether of
local or constitutional origin. If due to improper articulation
this must he corrected. If constitutional, and due to any of the
mineral poisons or scurvy, the system should be flooded with large
quantities of pure water. There is uothing better to rid the sys-
tem of poisons and impurities than flushing the blood with from
three to five quarts of pure water a day. Cathartics should be
employed. A Turkish hath should he used to open the ports of
the skin, at which time the masseur should be instructed to stim-
ulate the liver, kidneys, skin and peripheral nerves. If the
patient suffer from disease like syphilis, tuberculosis, diabetes,
Bright's disease, colds, including catarrh, nervous prostration,
amemia, etc., special treatment is indicated. Remove all deposits
and other irritants from around the teeth.

Two decades ago, I advocated the use of the following set of
scalers; nothing better has been produced since. They consist
of handles, shanks bent at different angles, and blades three-
cornered, so that they can be used in three directions without
removing the fingers from the tooth (Fig-. 70). These are all
delicately made, and tempered very hard. Sharp edges are
there retained. They will reach every point where tartar can
collect. After the deposits have been fairly well removed, the
gums may be syringed with hot water (Cravens) to remove all
debris. The gums should be saturated with tincture of iodin
( C S. I'. ) or iodin and aconite, in the following manner : Have a
number of wooden toothpicks ( Portuguese preferable) wound with
cotton, and kept in a little box. Saturate the cotton and paint
the gum as far as it will go. Throw this into the waste basket
and take another, and so on until the gums are well saturated.
From three to five picks will be required. The assistant can
keep these in order between patients. In such cases a different
massage Brush is to be used. One is here required that will so
lacerate and stimulate the gums as to relieve the congestions-.
This brush, made of coarser and stiffer bristles, should be used like

178

INTERSTITIAL GINGIVITIS.

the other. After two or three days the gums will contract, and
healthy circulation follow. Pain will now be experienced in the
gums. The massage must still be kept up. An astringent,
stimulating and general mouth wash, should be used in connec-
tion with the massage. The patient should return every other
day for further treatment with the iodin, or iodin and aconite
used as before. To reach an inflammation, chronic and deep-
seated, extending into the peridental membrane, periosteum and
alveolar process, there is nothing in medicine better than iodin,
or iodin and aconite. This, and this alone, will reach the deeper
inflammation. After a few treatments and constant use of the
massage brush, the gums will contract, and other deposits which

were overlooked at the first sitting will now be presented to
view. If the gums be very painful at the first sitting, no effort
should be made to remove the deposits until the inflammation
has, in a. measure, subsided. The iodin treatment and massage
should be conducted as suggested until the gums have been
reduced and the pain ceases. After they have been restored to
health, constant massage with the medium brush must be
employed two or three times a day. The patient should return
to the dentist as often as necessary (every month or two) to
have the gums examined, and for further direction.

TREATMENT. 1 79

As lias been already shown, chronic interstitial gingivitis may
extend only to the peridental membrane, to the periosteum, or it
may extend throughout the alveolar process with the absorption
of the hone the entire length of the root of the tooth. Pus
infection and serumal deposit may or may not take place. In
the early stages of this progressive inflammation, the first is prob-
able. If pus and deposits are present they can be treated with
signal success according to the symptoms and as hereinafter
explained. As already suggested, the gum massage brush must
he vigorously used to relieve the engorged tissues of blood.
Since absorption of the alveolar process depends upon irritation
and inflammation, this must be removed as quickly as possible.

In the treatment of deep-seated interstitial inflammation,
iodin or iodin and aconite has always been regarded by physi-
cians and surgeons as the best remedy. The gums should be
thoroughly saturated twice or thrice weekly, as already suggested.
If the alveolai' process be so absorbed that the tooth has become
loose, the ease is hopeless. In such unstable tissues, especially
when inflammation extends through the process and lacunar,
perforating canal absorption and halisteresis is going on, reversal
of the order so as to set the osteoblasts to tissue-building is
hardly to be expected. The tendency is to destroy and not
restore the alveolar process. In such cases the tooth must be
fastened to the other teeth perfectly tight to prevent motion in
any direction. The movement of the tooth in mastication inten-
sifies the irritation, which in time only increases the absorption.
Liberal use of iodin or iodin and aconite and the gum massage
brush is all that can be done to reduce the inflammation and
absorption as much as possible. The exfoliation is only a matter
of time. If the tooth or teeth cannot be retained perfectly tight.
no matter how healthy the surrounding tissues may be restored,
the irritation produced by the loose teeth will soon set up inflam-
mation in the surrounding tissues. The sooner the loose teeth
are removed the better. In no case can the bone tissue be
restored, if the matrix or cartilage be destroyed, since in this the
osteoblasts are located. If the matrix or cartilage be destroyed,
a fibrous union (such as occurs in the case of implanted teeth and
the imbedding of foreign bodies in the tissues of the body) only
is possible.

180 INTERSTITIAL GINGIVITIS.

If inflammation have extended into the periosteum, peri-
dental membrane and alveolar process, serumal calculi are fre-
quently deposited upon the roots of the teeth. When this has
taken place, the calculus must be removed. This should be
done with the utmost care, in order that adjacent tissues may not
be injured, or inflamed parts infected with pus germs. Since
dead bone is not present, the operator should confine his instru-
mentation entirely to the root or roots of the teeth, with as little
injury as possible to the adjacent tissues. The alveolar process
must under no consideration be touched. Riggs believed that
the edge of the alveolar process was always in a state of dis-
integration, and that it should be so scraped as to get a fresh
surface, on the principle of caries of bone. Many dentists are
operating in this manner at the present time. I have elsewhere
shown simple absorption and not caries is present. Such treat-

ment is wholly unnecessary and contraindicated. The object of
the removal is to allow the fibrous tissue of the peridental mem-
brane ( after health is restored ) to tighten about the root, which
cannot be accomplished when foreign substances are present.
Pushing instruments must never he used, but only such instru-
ments as have smooth and round backs, tempered very hard so as
to retain sharp edges. These instruments should be small, with
small points to reach depressions, and to be as universal as pos-
sible. Such an instrument is to be found in the spoon excavator
(Fig. 71). The shank can be bent to suit the operator. This is
to be carried gently along the length of the root and passed
over the deposit with a firm hand, resting the finger upon some
other teeth. The drawing motion is invariably to be from the
membrane, and toward the crown. The deposits are sealed off

TREATMENT. 181

painlessly. The round blade being larger than the shank, and
cutting- upon three edges, half of the root in both directions can
be circled without removing the instrument. A similar instru-
ment bent at the shank in the opposite direction may be used on
the other side. After all of the roots of the teeth have been
scaled, the spaces are to be syringed out with warm or hot
water (Cravens). The gums are to be thoroughly saturated
inside and out with iodin. The gum massage brush is to be used
thrice daily as before. The patient should return twice or thrice
a week for further instructions. The contracting gums will
assist greatly in revealing the deposit. If deposits still remain
on the roots (the appearance of the gums will indicate its pres-
ence) further use of the scalers is indicated. The delicate instru-
ments and the accustomed sense of touch will reveal the hidden
calculus.

With the precautions already noted, local anaesthesia is
unnecessary. The smooth, round surface of the back of the
instrument, if carefully inserted, will not produce pain.

If the gum be painful to the touch, or if the patient be
nervous and sensitive, application of tincture iodin may be used,
together with massage, for a few days before scaling is resorted
to. The sensitiveness will soon disappear, when the instrument
may lie inserted without difficulty.

A few years hence, the profession will regard a dentist whose
patients have pus oozing from the gums as a prehistoric relic and
the patient as an individual whose filth provokes the contempt of
his fellows. In this day of antisepsis, the dentist is as account-
able for pus infection of his patients as the physician or surgeon.

There is no more excuse for the dentist's patient being in-
fected than the surgeon's. If ordinary antiseptic precautions are
taken, pus infection will not often occur. Prevent inflammation
of the gum margin and pus infection cannot follow, no matter
how many germs be in the mouth. This is an absolute law of
general pathology. It has been proven by the experiments made
by Miller, G. T. Carpenter and myself on dogs, rabbits and man.

The illustrations of the progress of interstitial gingivitis teach
that only the mildest treatment is indicated. Harsh treatment
on the infiamed bone or fibrous tissue, either with instruments or
drugs, must not be employed. Heroic treatment, such as the

182 INTERSTITIAL GINGIVITIS.

indiscriminate application of sulphuric and lactic acid and sim-
ilar drugs in nearly or quite full strength, is not justified by the
surgical principles of today. No surgeon would think of making-
such an application to inflamed bone in other parts of the body
without he wished necrosis with a desired sequestrum. Much
less would the intelligent operator use such treatment in a transi-
tory structure which predisposed to destruction. In a number of
instances exfoliation of the anterior plate of the alveolar process
has resulted from this treatment, to say nothing of the intense
pain produced. J. M. Whitney 1 has had four cases in his prac-
tice in which serious results followed. The first indication is to
remove the cause. Instrumentation should be resorted to only
to remove tartar and calcic deposits. This must be done in such
a manner as not to infect the deeper inflamed tissue or carry the
products of inflammation into healthy tissue. The treatment of
infected tissue within and about the alveoli is not unlike treatment
of abscesses and ulceration elsewhere. Such drugs as are used
in abscesses and ulcers in other tissues are indicated here in the
same strength. If strong drugs be used they should not be per-
mitted to remain in the tissue, lest necrosis of the alveolar process
occur. They must be diluted or removed altogether after they
have accomplished their purpose. Very serious results have
occurred from careless use of drugs. When abscesses have
formed they should be opened and hydrogen peroxid — or, which
has answered my purpose equally well, hot water (Cravens) — is all
that is necessary. More difficult is treatment of ulceration of the
tissue near the root of the tooth. Ordinary cases will heal after
hot water or hydrogen peroxid have been applied. In some
cases the pus germs have followed the inflammation along the
course of the vessels quite a distance into the interstitial tissue.
In such cases they are difficult to reach. A small syringe
(George T. Carpenter's) may be employed, or the drug may be
carried to the part on the end of a long, thin orange-wood stick.
In all cases the drug must be directly applied to the part in order
to have beneficial results. Applications of iodin should be used,
as already suggested. Iodin carried to the ulcerated surface often
suffices to destroy the pus secretion. Ordinarily one or two
applications is sufficient. Occasionally calcic deposits are located

1 International Dental Journal, April, 1899.

TREATMENT. 183

in front of the infected surface and the drug does not reach the
part. In such eases the deposit must be removed. If the pus do
not cease at the first, second or even third application, this is not
because the drug is not sufficiently strong, Imt because it does not
reach the infected part. Continued applications of iodin exter-
nally and internally, carried well up between the roots of the
tooth and the alveolar process will, in time, produce the desired
result. When pus ceases to flow, antiseptic treatment must stop.
The iodin and massage treatment must then he pushed until the
interstitial inflammation has been reduced and the gums con-
tracted tightly about the necks of the teeth.

After the tissues have been placed in a healthy condition,
they will require the constant attention of the operator, since,
like other tissues of the body when once diseased, favorable con-
ditions will cause a recurrence. The patient must return to the
operator frequently so that he can advise as to the use of massage.

I have elsewhere shown that uric acid ( like lactic and other
acids, mercury, lead and brass poisoning) may produce local
irritation in a small number of cases, resulting in interstitial
gingivitis. Uric acid is absorbed into the blood and is thus car-
ried to all parts of the body. As mercury, lead, brass and potas-
sium iodide collect in the tissues of the alveolar process, on
account of the sln<;'o'ish blood supply, so does uric acid, setting
up inflammation. These cases are easily diagnosed, since, unlike
the ninety-four per cent of cases that begin at the gum margin
without pain and are of long standing, these set up a spontaneous
inflammation in an otherwise healthy alveolar process. This
may occur about one tooth, or more may be involved; usually it
involves the tooth or teeth standing alone or having improper or
no articulation. The inflammation is followed by acute pain.
If this be not reduced an abscess may, as elsewhere shown, form
at some locality about the alveolar process. Inflammation will
extend throughout the alveolar process and rapid absorption
result. The tooth will loosen in the socket. If systemic treat-
ment he not at once instituted, exfoliation of the tooth or teeth
shortly ensues. The first thing indicated in such cases is an
application of iodin to reduce inflammation and pain. The urine
for twenty-four hours should be secured for chemical analysis.

The materials and appliances necessary for the purpose of

184 INTEESTITIAL GINGIVITIS.

making an examination of the urine for uric acid are many and
the method requires considerable time. The dentist can do the
work, but it will be much more satisfactory (if he must know the
quantity eliminated each day) to send it to a competent chemist.
Should he desire to make the urine analysis, I should recom-
mend the method suggested by Bartley * in which he says, " The
estimation of uric acid is usually attended with much difficulty
and consumption of time. The author has devised the following
volumetric method, which is fairly rapid, reasonably accurate
and requires little skill. It can therefore claim a place as a
clinical method. The process is based upon the well-known
fact that uric acid is completely precipitated from its solutions
containing an excess of ammonium-magnesium mixture and
ammonium hydroxide, by silver nitrate. When the precipita-
tion is complete, the slightest trace of silver in solution is shown
by the dark color j>roduced in a drop of the clear solution by a
soluble sulphide." The method of procedure is thus explained,
should the uric acid excreted in twenty-four hours be less than .8
grams or 10.8 grains it is safe to say that it is retained in the
system.

Imperfect tissue metabolism, as V. A. Gudex, 2 of Milwaukee,
has shown, results in the formation of the following acids and
substances: uric, hippuric, oxaluric, carbonic, lactic and lac-
tates, caprylic, caproic, valerianic, butyric, propionic, acetic,
stearic, oleic, palmitic, formic, eholalic,. tuarilic, damaluric,
damalic, and succimic acids. Of these, the uric acid seems to act
least as an irritant. The urine, therefore, should be examined
for general acidity, the general treatment of which will accom-
plish all that is to be desired. A safe and delicate test can be
accomplished by determining the alkalinity of the urine, saliva,
perspiration, expectoration and dejection. The dentist is fortu-
nate in this because he has every convenience at hand. Lieb-
reich's methods of the use of plaster of paris plates as elaborated
by A. H. Hoy, 3 of Chicago, is most admirably adapted for this
purpose, since the test can be readily applied. To make the
plates, mix a very thin quantity of dental plaster to the con-

1 Medical Chemistry, page 641 ; fifth edition.

2 Items of Interest, May, 1891).

3 Eating and Drinking.

TREATMENT. ] 85

sistency of cream, care being taken to thoroughly incorporate
the plaster. Take two panes of window glass, cut four pieces of
wood three-sixteenths of an inch in thickness and place one at
each corner of the glass; now pour the plaster into the center,
place the other plate of glass above and press it down upon the
blocks of wood. By this method a very smooth surface can be
obtained. Make a round cutter out of tin, the size of a twenty-
five cent piece. Remove the upper piece by sliding it off, cut
out round disks just before the plaster hardens. These are pre-
pared in the following manner: A solution of litmus in 12
parts of water is rendered. alkaline or bright blue by adding a
few drops of aqua ammonia. After the disks have become per-
fectly hard, the smooth polished surface is to be painted with
the solution, using a camel's-hair brush. Two or three applica-
tions are to be made, until an even blue stain is obtained. Have
a solution of chemically pure sulphuric acid, two parts in five
hundred of distilled water, ready in a bottle, and a bottle of dis-
tilled water. To prepare the disk for the test, scrape one-half
of the dark blue surface of the plate until a slight blue sur-
face is obtained. This requires the removal of only a slight
amount, since the blue stain only penetrates a short dis-
tance. With a small brush, dipped into the acid, draw it quickly
over the surface exposed, giving a red appearance to the field
adjoining the blue. 1 A bit of cotton, wound around the end
of a toothpick wet with distilled water and applied to the
two colors, will produce no change, thus proving everything to
be in working order. The fluid to be tested — urine, saliva or
perspiration — may now lie applied. When possible, the exudate
must be applied to the test as soon as it leaves the body, care
being taken to apply a fixed amount each time. Apply the
fluid to be examined to both the blue and red fields. When
saliva is used, the mouth must be rinsed two or three times and
the quantity first sucked out of the ducts must not be used.
Fresh saliva direct from the glands should only be used. The
plates, alter they have been used, may be re-stained and used
indefinitely. The dentist should make repeated tests of the
secretions of healthy individuals under different conditions

1 It is almost impossible to obtain a satisfactory permanent red litmus. By this
method the red and blue fields stand out in bold contrast.

186 INTERSTITIAL GINGIVITIS.

before studying those of diseased conditions. This method is
a more delicate test than it is possible to make even with
litmus paper. Litmus paper often fails to reveal reaction,
which will be most obvious by this method.

The secretions of the body, if found to be acid, must be
placed in an amphoteric condition as soon as possible. An
amphoteric condition is a reaction of the urine, by which
both the blue and the red litmus are affected. If the red
becomes blue and the blue red it indicates that there is an
amphoteric reaction. The salt giving the alkaline reaction is
the trisodic phosphate ; that giving the acid reaction is the mon-
asodic phosphate. When a uniform color is produced it shows
that the alkaline and acid salts are being properly excreted in
proper amounts with no excess of free acid.

The normal urine specific gravity is 1018 to 1025. To
determine the specific gravity, the morning urine should be used.
If about 1018 or lower and acid, it is due to fermentation in
small intestines. In such cases avoid yeast bread, acid fruits,
wines, vinegar and all acids. If specific gravity is 1025 or
more and acid, avoid meats. From five to seven pints of pure
water should be taken each day, to flush the blood and kidneys
and thus cleanse the system. Certain patients, especially neu-
rasthenics, nervous dyspeptics and many lithsemics, have a
repulsion to pure water. The water can be adjusted to these
idiosyncrasies by the employment of lithia or other effervescent
tablets. The main object is to preserve in such cases the promi-
nent idea of the water being medicated. Local treatment, as
elsewhere described, should here be resorted to. Besides the use
of water, dietetics in dentistry involve chiefly a conservative
question.

Under most conditions of suboxidation and imperfect elimi-
nation, as elsewhere shown, the gums are forced to assume an
excretory energy to which they are unequal. As a consequence
a foundation is laid for interstitial gingivitis, which, in all of its
types, may seriously threaten the integrity of the teeth. Nay,
more, by furnishing a culture medium for pus microbes it may
threaten the general health, not only through systemic infec-
tion, but also through its interference with proper gastro-intestinal
digestion. Among the restrictions in diet which dental hygiene

TREATMENT. 187

demands is, first, a restriction in foods and water containing an

excess of lime salts, which produce tartar. As excess of foods
containing nitrogen, when aided by an imperfect assimilation of
the carbohydrates, tend to produce constitutional conditions like
lithaemia, gout, etc.. which affect tissue nutrition of the gums, these
foods require restriction and adaptation to the particular case.
While the constitutional condition underlying lithaemia markedly
predisposes to gum irritations and inflammations, its value as an
exciting cause is hut slight. Lactic acid, as has been elsewhere
pointed out, is a more marked local excitant. In the constitutional
production of lactic acid, ingestion of the carbohydrates without
assimilation plays a part. Scurvy, which may seriously threaten
the integrity of the gums, requires the usual dietetic treatment.
While there are indications of the untoward effects of infantile
scurvy on the gums, the pathology and consequences of it are
not as well known as those of scurvy in the adult. The
researches on scurvy in the infant tend to show that it results
from a monotony of diet rather than the absence of any article of
diet. The dietetics of dentistry, therefore, involve precisely the
same principles as do the treatment of the constitutional con-
ditions which are the predisposing factors of the gum disorders.
During the entire process of treatment (indeed before the
treatment begins) a suitable mouth wash should he used two or
three times a day. This should be composed of a germicide,
antiseptic disinfectant and deodorant, and should he used at the
time of the massage.

INDEX OF AUTHORS.

PAGE

Alexander, H. C. B 145

Allbright 3

Andrews, R. R 89

Arcovy 4

Barlow, Thomas 95

Barrett 174

Bartley 184

Black . 5, 34, 41, 47, 48, 51, 53, 5G, 98

Beodecker 174

Bondurant 91

Bon will 2, 157

Brown 2

Brubaker, A. B 08

Buzzard 97

Calve, Marshall de 2

Carpenter, G. T. 125, 165, L70,

181, 182

Cartright, Hamilton 4

Clowes 3

Coles, Oakley 4

Collins, J 66

Congdon 68

Cravens 181, 182

Cruveilier, C 92

Dana, C. L 97

Dickinson, Howship 78

Ebner, Von .... 56, 153, 158, 160

Eisenhart 159

Enderlin 76

Essig, C. J 3

Evans, W. A 123

Farrar, F. N 4

Fitzgerald 9, 68, 167

Flower, Alsop 14

Foster 11

Fuchard, H. A 2

Galippe . . 4,12,122,123,124,151

Geddings, H. D 75

Gray 37

Gudex, V. A 184

Hektoen, L 127, 155

Hertwig, 56, 146

Herzog, M 124

PAGE

Hirt 97

Hogben 94

Howell 77

Hoy, A. H. ........ 184

Ingersol, L. C 4

Izklai, Joseph 4

Jacobi 95

Jacobson . . 75

Joirac 2

Jourdain 2

Kaecker 2

Kaufinann . . .61, 154, 157, 158

Kirk 12, 68

Koch 12, 151

Kolliker .... 30,33,56,62, 161

Kuttner 169

Magitot . . - 2, 7, 53, 55, 57, 58, 91

Mailhol 11

Malasses 4

Malenfont 79

Miller. . 8,82,89,122,123,125,181

Mills 3

Minot 42, 53, 56, 146

Morgan, de 31

Niles, N. S 3

Noyes, Frederick 48

Patterson 4, 6, 8, 89

Pedley 6, 7

Pierce, C. N. . . . 8, 12, 37, 68, 96

Quain 10, 11

Raw Is, A. 4, 95

Rechlinghausen, Von 159

Reese 4

Reeves 68

Rehwinkle 3

Rhein 68, 175

Riggs, J.T 2, 180

Robin 53, 55, 57, 58, 91

Rokitansky 169

Rose 54

Salisbury, J. H. . . . 69,71, 7'.'

Sayre, Charles E 14

Schefi 2

190

INDEX OF AUTHORS.

PAGE

Scheheoetskey 78

Schmidt, C 73, 74, 70, 78

Serres 47

Sirletti 3

Starr, A. R 5

Stevenson 78

Sudduth, W. X. ... 5, 6, 7, 8, 161

Sutton, Bland 7

Talbot, E. S 5, 47

Tomes . .
Yolkmann
Virchow .
Waldeyer
Walker . .

Wesener, J. A 09, 70

Whitney, J. M 182

Zawadsky 76

Ziegler 28, 158

PAGE

. . 27, 31, 175

31, 62, 63, 153, 160

. . . 169, 170

INDEX OF SUBJECTS.

PAGE

Acadians, Teeth of 1

Alveolar Process 21

Absorption of 147

Absorption 157

Absorption and Trophic

Change 162

Changes 149

Dermal Bones 96

Germ Infection . . . . 96

Hypei'trophy of 29

Antimony 144

Arsenic 144

Bone Absorption 59

Bone Building 59

Brass 144

Interstitial Gingivitis ... 94

Bromides 145

Calcic Deposits _ 168

Calcospheritea 41, 133

Calculi, Salivary 78

Carnivora, Interstitial Gingivitis in . 14
Catarrhal Idiosyncrasy .... 5
Cave Dwellers, Teeth of ... . 1

Cementoblasts 42

Cementoclasts 61

Children, Degenerate 89

Diathetic 89

Interstitial Gingivitis in . . 81

Neurotic 89

Pyorrhoea in 89

Debris, Epithelial 55

Dental Operations and Alveolar Pro-
cess 150

and Bone Absorption . .150

Dental Shelf 55, 56

Degeneracy and Degenerate Tissues . S7

Dentitions, The Three 84

Dogs, Interstitial Gingivitis in . 14, 98
Mercuric Interstitial Gingi-
vitis in 117

Pyorrhoea Alveolaris in . . 98
Ebner, Von, Vessels of .... 31
Egyptians, Teeth of 1

PAGE

Embryology of the Tooth .... 46
Endarteritis Obliterans .... 154
and Tuberculosis .... 155
Exanthemata and Catarrhal Gingi-
vitis 7

Follicle, The Dental 55

Gingivitis 5

Expulsive 11

Interstitial 9

and Pyorrhoea 9

Glands of Mucous and Peridental

Membranes 47

Greeks, Teeth of 1

Gums 42

Halisteresis . . . . 61, 62, 153, 158

Haversian Canals 30

Heredity 13

Interstitial Gingivitis . . . . 10, 12

Antimony 144

Arsenic 144

Atavism and 83

Auto-Intoxication and ... 66

Bacteriology of 122

Brass 144

Bromide 145

Carnivora in 14

Causes 12

Degeneracy and 86

Dogs 98

Environment and .... 84

Heredity and 83

Heredity in 13

Inorganic Salts and . 73

Iodide 145

Lactic Acid and 152

Mercuric 142

In Dogs 117

Nerve Phases of .... 13

Pathogeny of 151

Plumbic 143

Pyorrhoea Alveolaris and . . 162
Scorbutic in Man . . . .127
Scurvy and . . . 13, 65, 94

192

INDEX OF SUBJECTS.

PAGE

Interstitial Gingivitis —

Tartar and 148

Theories of 65

Toxic Causes of . . . .13, 92

Treatment ....... 172

Tropho-Neuroses and . . 66, 92

Uric Acid and 68

Iodides 145

Jaw, Evolution of 149

Evolutionary Changes in . . 20
Racial Changes in .... 20
Lake Dwellers, Teeth of ... . 1
Lactic Acid and Interstitial Gingi-
vitis 152

Lacunar Absorption .... 62, 153

Lead 143

Interstitial Gingivitis and . . 94
Locomotor Ataxia and Gum Dis-
order 13

Mercury 142

Interstitial Gingivitis and . 93
Mouth Breathing and Catarrhal Gin-
givitis 7

Mucous Membrane, Glands of 47

Histology of 42

Mucus, Bactericidal Function of . . 88

Odontoblasts 42

Osteoblasts 42

Osteoclasts 61

Osteomalacia .... 62, 146, 159
Papillary Layer, Comparative Anat-
omy 47

Paretic Dementia and Gum Dis-
order 13

Perforating Canal Absorption . 62, 153
Pericementitis Phagadenica ... 5

Peridental Membrane 33

< Hands of 47

Inflammation 1

Periosteum 33

Periostitis Alveo-Dentalis ... 2

Dentalis 2

Pockets and Interstitial Gingivitis . 152

PAGE

Potassium Iodid and Interstitial

Gingivitis 94

Pregnancy and Osteomalacia . . . 159

Primitive Races, Teeth of ... 1

Pyorrhcea Alveolaris, Bacteriology of 162

Catarrhal Idiosyncrasy . . 5

Causes of 2

Constitutional Causes . 3, 4, 5
Constitutional Effects of . . 167

Degeneracy and 5

Dogs 98

Eruptive Fevers .... 7

History 2

Intestinal Disorders from . . 167

Lactic Acid 8

Nervous Causes 3

Parasites and 8

Pathology of 6, 7

Syphilis and 8

Systemic Disease and ... 8

Uric Acid and 8

Scurvy 96, 127

Sodium Chloride and Interstitial

Gingivitis 95

Stomatitis Catarrhalis 6

Teeth, Changes in 146

Changes in Position of . . .28

Decay of 147

Embryology of 146

Irregularities of 148

Periods of Evolution . . . 146
Periods of Involution . . . 146
Trophic Disorders of ... 96

Third Molar 149

Disappearance of .... 21

Tooth Embryology 42, 53

Form Changes 149

Transitory Structures . . . .20, 147

Tropho-Neuroses 13, 96

Ulitis 11

Uric Acid and Pyorrhoea Alveolaris 3, 8
Volkmann's Canals 31

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